SwePub - search: WFRF:(Li Xiujuan)

Enumeration	Reference	Cover	Find
1.	He, Qi, et al. (author) Pericyte dysfunction due to Shb gene deficiency increases B16F10 melanoma lung metastasis 2020 In: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 147:9, s. 2634-2644 Journal article (peer-reviewed)abstract Intravasation, vascular dissemination and metastasis of malignant tumor cells require their passage through the vascular wall which is commonly composed of pericytes and endothelial cells. We currently decided to investigate the relative contribution of these cell types to B16F10 melanoma metastasis in mice using an experimental model of host Shb gene (Src homology 2 domain containing protein B) inactivation. Conditional inactivation of Shb in endothelial cells using Cdh5-CreERt2 resulted in decreased tumor growth, reduced vascular leakage, increased hypoxia and no effect on pericyte coverage and lung metastasis. RNAseq of tumor endothelial cells from these mice revealed changes in cellular components such as adherens junctions and focal adhesions by gene ontology analysis that were in line with the observed effects on leakage and junction morphology. Conditional inactivation of Shb in pericytes using Pdgfrb-CreERt2 resulted in decreased pericyte coverage of small tumor vessels with lumen, increased leakage, aberrant platelet-derived growth factor receptor B (PDGFRB) signaling and a higher frequency of lung metastasis without concomitant effects on tumor growth or oxygenation. Flow cytometry failed to reveal immune cell alterations that could explain the metastatic phenotype in this genetic model of Shb deficiency. It is concluded that proper pericyte function plays a significant role in suppressing B16F10 lung metastasis.
2.	Li, Fusheng, 1985-, et al. (author) Electroless Plating of NiFeP Alloy on the Surface of Silicon Photoanode for Efficient Photoelectrochemical Water Oxidation 2020 In: ACS Applied Materials and Interfaces. - : American Chemical Society (ACS). - 1944-8244 .- 1944-8252. ; 12:10, s. 11479-11488 Journal article (peer-reviewed)abstract N- type silicon is a kind of semiconductor with a narrow band gap that has been reported as an outstanding light-harvesting material for photoelectrochemical (PEC) reactions. Decorating a thin catalyst layer on the n-type silicon surface can provide a direct and effective route toward PEC water oxidation. However, most of catalyst immobilization methods for reported n-type silicon photoanodes have been based on energetically demanding, time-consuming, and high-cost processes. Herein, a high-performance NiFeP alloy (NiFeP)-decorated n-type micro-pyramid silicon array (n-Si) photoanode (NiFeP/n-Si) was prepared by a fast and low-cost electroless deposition method for light-driven water oxidation reaction. The saturated photocurrent density of NiFeP/n-Si can reach up to similar to 40 mA cm(-2) and a photocurrent density of 15.5 mA cm(-2) can be achieved at 1.23 V-RHE under light illumination (100 mW cm(-2), AM1.5 filter), which is one of the most promising silicon-based photoanodes to date. The kinetic studies showed that the NiFeP on the silicon photoanodes could significantly decrease the interfacial charge recombination between the n-type silicon surface and electrolyte.
3.	Li, Wenlong, et al. (author) A bio-inspired coordination polymer as outstanding water oxidation catalyst via second coordination sphere engineering 2019 In: Nature Communications. - : NATURE PUBLISHING GROUP. - 2041-1723. ; 10 Journal article (peer-reviewed)abstract First-row transition metal-based catalysts have been developed for the oxygen evolution reaction (OER) during the past years, however, such catalysts typically operate at overpotentials (eta) significantly above thermodynamic requirements. Here, we report an iron/ nickel terephthalate coordination polymer on nickel form (NiFeCP/NF) as catalyst for OER, in which both coordinated and uncoordinated carboxylates were maintained after electrolysis. NiFeCP/NF exhibits outstanding electro-catalytic OER activity with a low overpotential of 188 mV at 10 mA cm(-2) in 1.0 KOH, with a small Tafel slope and excellent stability. The pH-independent OER activity of NiFeCP/NF on the reversible hydrogen electrode scale suggests that a concerted proton-coupled electron transfer (c-PET) process is the rate-determining step (RDS) during water oxidation. Deuterium kinetic isotope effects, proton inventory studies and atom-proton-transfer measurements indicate that the uncoordinated carboxylates are serving as the proton transfer relays, with a similar function as amino acid residues in photosystem II (PSII), accelerating the proton-transfer rate.
4.	Wu, Xiujuan, et al. (author) Exploration of electrocatalytic water oxidation properties of NiFe catalysts doped with nonmetallic elements (P, S, Se) 2021 In: International journal of hydrogen energy. - : Elsevier BV. - 0360-3199 .- 1879-3487. ; 46:79, s. 38992-39002 Journal article (peer-reviewed)abstract The introduction of non-metallic atoms (P, S, Se) has emerged as an effective way to improve the catalytic activity of transition metal based layered double hydroxides (LDHs) for oxygen evolution reaction. However, objective comparisons of the performance of heteroelement-doped catalysts are complicated by the lack of standardization both in the electrochemical tests and physicochemical analysis. Herein, we use a unified protocol for evaluating the catalytic activities of heteroelement-doped NiFe-LDHs and explore the reasons for the differences in their catalytic performance. Some regular results are found from comparing the properties of the heteroelement-doped catalysts: (1) the introduction of P/S/Se can optimize the redox behaviors of Ni species, which is conducive to regulating adsorption energy of intermediates and the formation of high-valent active sites; (2) the specific area of catalysts was expanded after heteroelements doping, ensuring a more favorable structure for heterogeneous catalysis; (3) All P/S/Se-doped catalysts showed better activities when compared to the original NiFe LDHs in alkaline solutions, and the catalysts doped with S showed the best performance (Se < P < S).
5.	Wu, Xiujuan, et al. (author) Hierarchically Structured FeNiOxHy Electrocatalyst Formed by In Situ Transformation of Metal Phosphate for Efficient Oxygen Evolution Reaction 2018 In: ChemSusChem. - : WILEY-V C H VERLAG GMBH. - 1864-5631 .- 1864-564X. ; 11:11, s. 1761-1767 Journal article (peer-reviewed)abstract A simple and low-cost fabrication method is needed to obtain effective and robust heterogeneous catalysts for the oxygen evolution reaction (OER). In this study, an electrocatalyst FeNiOxHy with a hierarchical structure is synthesized on nickel foam by a simple fabrication method through anion exchange from a metal phosphate to a metal hydroxide. The as-fabricated FeNiOxHy electrode requires overpotentials of 206 and 234 mV to deliver current densities of 10 and 50 mAcm(-2), respectively. The catalytic performance of FeNiOxHy is superior to that of most previously reported FeNi-based catalysts, including NiFe layered double hydroxide. The catalyst also shows good long-term durability at a current density of 50 mA cm(-2) over 50 h with no activity decay under 1 m KOH. By comparison to the directly electrodeposited FeNi hydroxide in morphology and electrochemical properties, the improved activity of the catalyst could be mainly attributed to an enhancement of its intrinsic activity, which was caused by the anion exchange of phosphate to (oxy)hydroxide. Further studies by cyclic voltammetry indicated a stronger interaction between Ni and Fe from the negative shift of the oxidation peak of Ni2+/Ni3+ in comparison with reported FeNiOxHy, which promoted the generation of active Ni3+ species more easily. This work may provide a new approach to the simple preparation of effective and robust OER catalysts by anion exchange.
6.	Yang, Hao, et al. (author) Improving the performance of water splitting electrodes by composite plating with nano-SiO2 2018 In: Electrochimica Acta. - : Pergamon Press. - 0013-4686 .- 1873-3859. ; 281, s. 60-68 Journal article (peer-reviewed)abstract The electrochemical splitting of water requires efficient functional electrodes. Herein, we report the fabrication of electrocatalyst consisted of an electrodeposited NiFeP alloy film which was composite plated with nano-SiO2 on nickel foam. The structure and morphology of the film were characterized by X-ray photoelectron spectroscopy (XPS), scanning electron microscopy (SEM) and transmission electron microscopy (TEM). The results showed that the surface area of this NiFeP-SiO2 co-deposition alloy film can be significantly increased after electrochemical etching in a KOH solution. The water splitting properties of the alloy film were evaluated using electrochemistry. By using the NiFeP-SiO2/NF(Etched) as a bifunctional electrode, total water splitting has been demonstrated in a two-electrode cell with a current density of 10 mAcm(-2) at an applied voltage of 1.57 V, which exhibited enhanced water splitting activity in comparison to the analogue cell using the pristine NiFeP/NF electrode.
7.	Bhattacharya, Resham, et al. (author) Distinct role of PLC{beta}3 in VEGF-mediated directional migration and vascular sprouting 2009 In: Journal of Cell Science. - : The Company of Biologists. - 0021-9533 .- 1477-9137. ; 122:7, s. 1025-1034 Journal article (peer-reviewed)abstract Endothelial cell proliferation and migration is essential to angiogenesis. Typically, proliferation and chemotaxis of endothelial cells is driven by growth factors such as vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). VEGF activates phospholipases (PLCs) - specifically PLCgamma1 - that are important for tubulogenesis, differentiation and DNA synthesis. However, we show here that VEGF, specifically through VEGFR2, induces phosphorylation of two serine residues on PLCbeta3, and this was confirmed in an ex vivo embryoid body model. Knockdown of PLCbeta3 in HUVEC cells affects IP3 production, actin reorganization, migration and proliferation; whereas migration is inhibited, proliferation is enhanced. Our data suggest that enhanced proliferation is precipitated by an accelerated cell cycle, and decreased migration by an inability to activate CDC42. Given that PLCbeta3 is typically known as an effector of heterotrimeric G-proteins, our data demonstrate a unique crosstalk between the G-protein and receptor tyrosine kinase (RTK) axes and reveal a novel molecular mechanism of VEGF signaling and, thus, angiogenesis.
8.	Cébe-Suarez, Stéphanie, et al. (author) Orf virus VEGF-E NZ2 promotes paracellular NRP-1/VEGFR-2 coreceptor assembly via the peptide RPPR 2008 In: The FASEB Journal. - : Wiley. - 0892-6638 .- 1530-6860. ; 22:8, s. 3078-3086 Journal article (peer-reviewed)abstract Vascular endothelial growth factors (VEGFs) interact with the receptor tyrosine kinases (RTKs) VEGFR-1, -2, and -3; neuropilins (NRPs); and heparan sulfate (HS) proteoglycans. VEGF RTKs signal to downstream targets upon ligand-induced tyrosine phosphorylation, while NRPs and HS act as coreceptors that lack enzymatic activity yet modulate signal output by VEGF RTKs. VEGFs exist in various isoforms with distinct receptor specificity and biological activity. Here, a series of mammalian VEGF-A splice variants and orf virus VEGF-Es, as well as chimeric and mutant VEGF variants, were characterized to determine the motifs required for binding to NRP-1 in the absence (VEGF-E) or presence (VEGF-A(165)) of an HS-binding sequence. We identified the carboxyterminal peptides RPPR and DKPRR as the NRP-1 binding motifs of VEGF-E and VEGF-A, respectively. RPPR had significantly higher affinity for NRP-1 than DKPRR. VEGFs containing an RPPR motif promoted HS-independent coreceptor complex assembly between VEGFR-2 and NRP-1, independent of whether these receptors were expressed on the same or separate cells grown in cocultures. Functional studies showed that stable coreceptor assembly by VEGF correlated with its ability to promote vessel formation in an embryoid body angiogenesis assay.
9.	Edholm, Dan, et al. (author) Fate and Performance of flk1-/- Endothelial Precursors Other publication (other academic/artistic)
10.	Edholm, Dan, 1972- (author) VEGFR-2 in Endothelial Differentiation and Vascular Organization 2008 Doctoral thesis (other academic/artistic)abstract The cardiovascular system is the first functional organ to develop during embryogenesis. As the embryo reaches above a certain size, passive diffusion of gases and nutrients is no longer compatible with efficient growth. During embryogenesis, endothelial progenitor cells (angioblasts) are recruited from the primitive streak mesoderm and instructed to express vascular endothelial growth factor receptor-2 (VEGFR-2). This thesis examines the roles played by VEGFR-2 in the events through which a subpopulation of embryonic stem (ES) cells differentiate into endothelial cells and form the vasculature. We show that ES cells gene targeted for VEGFR-2 (flk1-/-) develop immature endothelial cells (ECs), precursors, when differentiated in vitro as embryoid bodies (EBs). The flk1-/- ECs are unresponsive to VEGF-stimulation and consistently fail to form vessels. However, when co-cultured with wild type ES cells in chimeric EBs, flk1-/- endothelial precursors are guided by wild type ECs to form transient, chimeric vascular structures. Use of lentivirus in an add-back approach allowed reconstitution of VEGFR-2 expression in flk1-/- ES cells, and rescue of vasculogenesis and sprouting angiogenesis. We propose that recruitment to the endothelial lineage is not dependent on VEGFR-2, although this receptor tyrosine kinase appears indispensible for EC integrity, survival and for differentation of endothelial precursors into mature ECs formating a stable vasculature. Neuropilin-1 (NRP1) and heparan sulfate proteoglycans (HSPGs) function as co-receptors for VEGFs. The co-receptors influence, qualitatively and quantitatively, the intracellular signal relayed by VEGFR-2 but it is unclear how. We examined the contribution of NRP1 to VEGFR-2 signaling in EB cultures, in zebrafish and in mice. Only NRP1-binding VEGFs were able to promote sprouting angiogenesis and formation of properly branched vascular tubes, supported by pericytes. Downstream of VEGFR-2/NRP1 activation, we identified recruitment of p38MAPK in signal transduction regulating sprouting angiogenesis.
11.	Fang, Zhiyong, et al. (author) Selective Electro-oxidation of Alcohols to the Corresponding Aldehydes in Aqueous Solution via Cu(III) Intermediates from CuO Nanorods 2021 In: ACS Sustainable Chemistry and Engineering. - : American Chemical Society (ACS). - 2168-0485. ; 9:35, s. 11855-11861 Journal article (peer-reviewed)abstract Electrochemical oxidation using renewable energy is an attractive strategy that provides a sustainable and mild approach for biomass transformation. Herein, the electrocatalytic oxidation of furfuryl alcohol in an aqueous solution was investigated using CuO nanorods. Two kinds of Cu-III intermediates, namely, (CuO2)(-) and (Cu2O6)(6-), were detected on the surface of the working electrode. (Cu2O6)(6-), generated in the potential range of 1.35-1.39 V versus the reversible hydrogen electrode (RHE), induced the oxidation of furfuryl alcohol to furaldehyde with a yield of >= 98%. (CuO2)(-), generated at a potential greater than 1.39 V versus RHE, which led to the oxidation of furfuryl alcohol to 2-furoic acid with a yield of >= 99%. Furthermore, the Cu-III-catalyzed system exhibited a measure of universal applicability, wherein (Cu2O6)(6-) and (CuO2)(-) induced the highly selective electro-oxidation of benzyl alcohol, vanillyl alcohol, and 4-pyridinemethanol to yield the corresponding aldehydes and acids, respectively.
12.	Fernandez-Alonso, R., et al. (author) p73 is required for endothelial cell differentiation, migration and the formation of vascular networks regulating VEGF and TGF beta signaling 2015 In: Cell Death and Differentiation. - : Springer Science and Business Media LLC. - 1350-9047 .- 1476-5403. ; 22:8, s. 1287- Journal article (peer-reviewed)abstract Vasculogenesis, the establishment of the vascular plexus and angiogenesis, branching of new vessels from the preexisting vasculature, involves coordinated endothelial differentiation, proliferation and migration. Disturbances in these coordinated processes may accompany diseases such as cancer. We hypothesized that the p53 family member p73, which regulates cell differentiation in several contexts, may be important in vascular development. We demonstrate that p73 deficiency perturbed vascular development in the mouse retina, decreasing vascular branching, density and stability. Furthermore, p73 deficiency could affect non endothelial cells (ECs) resulting in reduced in vivo proangiogenic milieu. Moreover, p73 functional inhibition, as well as p73 deficiency, hindered vessel sprouting, tubulogenesis and the assembly of vascular structures in mouse embryonic stem cell and induced pluripotent stem cell cultures. Therefore, p73 is necessary for EC biology and vasculogenesis and, in particular, that DNp73 regulates EC migration and tube formation capacity by regulation of expression of pro-angiogenic factors such as transforming growth factor-beta and vascular endothelial growth factors. DNp73 expression is upregulated in the tumor environment, resulting in enhanced angiogenic potential of B16-F10 melanoma cells. Our results demonstrate, by the first time, that differential p73-isoform regulation is necessary for physiological vasculogenesis and angiogenesis and DNp73 overexpression becomes a positive advantage for tumor progression due to its pro-angiogenic capacity.
13.	Hayashi, Makoto, et al. (author) VE-PTP regulates VEGFR2 activity in stalk cells to establish endothelial cell polarity and lumen formation 2013 In: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 4, s. 1672- Journal article (peer-reviewed)abstract Vascular endothelial growth factor (VEGF) guides the path of new vessel sprouts by inducing VEGF receptor-2 activity in the sprout tip. In the stalk cells of the sprout, VEGF receptor-2 activity is downregulated. Here, we show that VEGF receptor-2 in stalk cells is dephosphorylated by the endothelium-specific vascular endothelial-phosphotyrosine phosphatase (VE-PTP). VE-PTP acts on VEGF receptor-2 located in endothelial junctions indirectly, via the Angiopoietin-1 receptor Tie2. VE-PTP inactivation in mouse embryoid bodies leads to excess VEGF receptor-2 activity in stalk cells, increased tyrosine phosphorylation of VE-cadherin and loss of cell polarity and lumen formation. Vessels in ve-ptp(-/-) teratomas also show increased VEGF receptor-2 activity and loss of endothelial polarization. Moreover, the zebrafish VE-PTP orthologue ptp-rb is essential for polarization and lumen formation in intersomitic vessels. We conclude that the role of Tie2 in maintenance of vascular quiescence involves VE-PTP-dependent dephosphorylation of VEGF receptor-2, and that VEGF receptor-2 activity regulates VE-cadherin tyrosine phosphorylation, endothelial cell polarity and lumen formation.
14.	He, Qi, et al. (author) The Cdh5-CreERT2 transgene causes conditional Shb gene deletion in hematopoietic cells with consequences for immune cell responses to tumors 2019 In: Scientific Reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 9 Journal article (peer-reviewed)abstract The tamoxifen-responsive conditional Cdh5-CreERT2 is commonly used for endothelial cell specific conditional deletion of loxP-flanked gene sequences. To address the role of endothelial cell Shb gene for B16F10 melanoma immune responses, tamoxifen-injected Cdh5-CreERT2/WT and Cdh5-CreERT2/Shbflox/flox mice received subcutaneous tumor cell injections. We observed a decrease of tumor myeloid cell Shb mRNA in the tamoxifen treated Cdh5-CreERT2/Shbflox/flox mice, which was not present when the mice had undergone a preceding bone marrow transplantation using wild type bone marrow. Differences in CD4+/FoxP3+ Tregs were similarly abolished by a preceding bone marrow transplantation. In ROSA26-mTmG mice, Cdh5-CreERT2 caused detectable floxing in certain bone marrow populations and in spleen cells. Floxing in bone marrow could be detected two months after tamoxifen treatment. In the spleen, however, floxing was undetectable two months after tamoxifen treatment, suggesting that Cdh5-CreERT2 is operating in a non-renewable population of hematopoietic cells in this organ. These data suggest that conditional gene deletion in hematopoietic cells is a potential confounder in experiments attempting to assess the role of endothelial specific effects. A cautious approach to achieve an endothelial-specific phenotype would be to adopt a strategy that includes a preceding bone marrow transplantation.
15.	Jamalpour, Maria, et al. (author) Disparate effects of Shb-gene deficiency on disease characteristics in murine models of myeloid, B-cell and T-cell leukemia 2018 In: Tumor Biology. - : IOS Press. - 1010-4283 .- 1423-0380. ; 40:4, s. 1-13 Journal article (peer-reviewed)abstract The Src homology-2 domain protein B is an adaptor protein operating downstream of tyrosine kinases. The Shb gene knockout has been found to accelerate p210 Breakpoint cluster region-cAbl oncogene 1 tyrosine kinase-induced leukemia. In human myeloid leukemia were tumors with high Src homology-2 domain protein B mRNA content, tumors were, however, associated with decreased latency and myeloid leukemia exhibiting immune cell characteristics. Thus, the aim of this study was to investigate the effects of Shb knockout on the development of leukemia in three additional models, that is, colony stimulating factor 3 receptor-T618I–induced neutrophilic leukemia, p190 Breakpoint cluster region-cAbl oncogene 1 tyrosine kinase-induced B-cell leukemia, and G12D-Kras-induced T-cell leukemia/thymic lymphoma. Wild-type or Shb knockout bone marrow cells expressing the oncogenes were transplanted to bone marrow–deficient recipients. Organs from moribund mice were collected and further analyzed. Shb knockout increased the development of CSF3RT618I-induced leukemia and increased the white blood cell count at the time of death. In the p190 Breakpoint cluster region-cAbl oncogene 1 tyrosine kinase B-cell model, Shb knockout reduced white blood cell counts without affecting latency, whereas in the G12D-Kras T-cell model, thymus size was increased without major effects on latency, suggesting that Shb knockout accelerates the development thymic lymphoma. Cytokine secretion plays a role in the progression of leukemia, and consequently Shb knockout bone marrows exhibited lower expression of granulocyte colony stimulating factor and interleukin 6 in the neutrophilic model and interleukin 7 and chemokine C-X-C motif ligand 12 (C-X-C motif chemokine 12) in the B-cell model. It is concluded that in experimental mouse models, the absence of the Shb gene exacerbates the disease in myeloid leukemia, whereas it alters the disease characteristics without affecting latency in B- and T-cell leukemia. The results suggest a role of Shb in modulating the disease characteristics depending on the oncogenic insult operating on hematopoietic cells. These findings help explain the outcome of human disease in relation to Src homology-2 domain protein B mRNA content.
16.	Jamalpour, Maria, et al. (author) Tumor SHB gene expression affects disease characteristics in human acute myeloid leukemia 2017 In: Tumor Biology. - : IOS Press. - 1010-4283 .- 1423-0380. ; 39:10 Journal article (peer-reviewed)abstract The mouse Shb gene coding for the Src Homology 2-domain containing adapter protein B has recently been placed in context of BCRABL1-induced myeloid leukemia in mice and the current study was performed in order to relate SHB to human acute myeloid leukemia (AML). Publicly available AML databases were mined for SHB gene expression and patient survival. SHB gene expression was determined in the Uppsala cohort of AML patients by qPCR. Cell proliferation was determined after SHB gene knockdown in leukemic cell lines. Despite a low frequency of SHB gene mutations, many tumors overexpressed SHB mRNA compared with normal myeloid blood cells. AML patients with tumors expressing low SHB mRNA displayed longer survival times. A subgroup of AML exhibiting a favorable prognosis, acute promyelocytic leukemia (APL) with a PMLRARA translocation, expressed less SHB mRNA than AML tumors in general. When examining genes co-expressed with SHB in AML tumors, four other genes (PAX5, HDAC7, BCORL1, TET1) related to leukemia were identified. A network consisting of these genes plus SHB was identified that relates to certain phenotypic characteristics, such as immune cell, vascular and apoptotic features. SHB knockdown in the APL PMLRARA cell line NB4 and the monocyte/macrophage cell line MM6 adversely affected proliferation, linking SHB gene expression to tumor cell expansion and consequently to patient survival. It is concluded that tumor SHB gene expression relates to AML survival and its subgroup APL. Moreover, this gene is included in a network of genes that plays a role for an AML phenotype exhibiting certain immune cell, vascular and apoptotic characteristics.
17.	Kawamura, Harukiyo, et al. (author) Neuropilin-1 in regulation of VEGF-induced activation of p38MAPK and endothelial cell organization 2008 In: Blood. - : American Society of Hematology. - 0006-4971 .- 1528-0020. ; 112:9, s. 3638-49 Journal article (peer-reviewed)abstract Vascular endothelial growth factor (VEGF)-A regulates vascular development and angiogenesis. VEGF isoforms differ in ability to bind coreceptors heparan sulfate (HS) and neuropilin-1 (NRP1). We used VEGF-A165 (which binds HS and NRP1), VEGF-A121 (binds neither HS nor NRP1), and parapoxvirus VEGF-E-NZ2 (binds NRP1 but not HS) to investigate the role of NRP1 in organization of endothelial cells into vascular structures. All 3 ligands induced similar level of VEGFR-2 tyrosine phosphorylation in the presence of NRP1. In contrast, sprouting angiogenesis in differentiating embryonic stem cells (embryoid bodies), formation of branching pericyte-embedded vessels in subcutaneous matrigel plugs, and sprouting of intersegmental vessels in developing zebrafish were induced by VEGF-A165 and VEGF-E-NZ2 but not by VEGF-A121. Analyses of recombinant factors with NRP1-binding gain- and loss-of-function properties supported the conclusion that NRP1 is critical for VEGF-induced sprouting and branching of endothelial cells. Signal transduction antibody arrays implicated NRP1 in VEGF-induced activation of p38MAPK. Inclusion of the p38MAPK inhibitor SB203580 in VEGF-A165-containing matrigel plugs led to attenuated angiogenesis and poor association with pericytes. Our data strongly indicate that the ability of VEGF ligands to bind NRP1 influences p38MAPK activation, and formation of functional, pericyte-associated vessels.
18.	Kawamura, Harukiyo, et al. (author) Vascular endothelial growth factor (VEGF)-A165b is a weak in vitro agonist for VEGF receptor-2 due to lack of coreceptor binding and deficient regulation of kinase activity 2008 In: Cancer Research. - 0008-5472 .- 1538-7445. ; 68:12, s. 4683-4692 Journal article (peer-reviewed)abstract Vascular endothelial growth factor (VEGF)-A165b is a COOH-terminal splice variant of VEGF-A that has been implicated in negative regulation of angiogenesis. We compared the properties of VEGF-A165b with those of VEGF-A121, VEGF-A145, and VEGF-A165. Induction of tyrosine phosphorylation sites in VEGFR-2 differed between the VEGF ligands as determined by tryptic phosphopeptide mapping and by use of phosphosite-specific antibodies. VEGF-A165b was considerably poorer in inducing phosphorylation of the positive regulatory site Y1052 in VEGFR-2. Whereas this did not affect activation of VEGFR-2 in vitro, we show that VEGF-A165b failed to induce vasculogenesis and sprouting angiogenesis in differentiating embryonic stem cells and vascularization of s.c. Matrigel plugs. In addition, the ability of the different VEGF ligands to induce angiogenesis correlated with their abilities to bind the VEGF coreceptor neuropilin 1 (NRP1). Our data indicate that loss of VEGFR-2/NRP1 complex formation and Y1052 phosphorylation contribute to the lack of angingenic properties of VEGF-A165b.
19.	Koch, Sina, et al. (author) Signal transduction by vascular endothelial growth factor receptors 2011 In: Biochemical Journal. - 0264-6021 .- 1470-8728. ; 437, s. 169-183 Research review (peer-reviewed)abstract VEGFs (vascular endothelial growth factors) control vascular development during embryogenesis and the function of blood vessels and lymphatic vessels in the adult. There are five related mammalian ligands, which act through three receptor tyrosine kinases. Signalling is modulated through neuropilins, which act as VEGF co-receptors. Heparan sulfate and integrins are also important modulators of VEGF signalling. Therapeutic agents that interfere with VEGF signalling have been developed with the aim of decreasing angiogenesis in diseases that involve tissue growth and inflammation, such as cancer. The present review will outline the current understanding and consequent biology of VEGF receptor signalling.
20.	Lanner, Fredrik, et al. (author) Hypoxia-Induced Arterial Differentiation Requires Adrenomedullin and Notch Signaling 2013 In: Stem Cells and Development. - : Mary Ann Liebert Inc. - 1547-3287 .- 1557-8534. ; 22:9, s. 1360-1369 Journal article (peer-reviewed)abstract Hypoxia (low oxygen) and Notch signaling are 2 important regulators of vascular development, but how they interact in controlling the choice between arterial and venous fates for endothelial cells during vasculogenesis is less well understood. In this report, we show that hypoxia and Notch signaling intersect in promotion of arterial differentiation. Hypoxia upregulated expression of the Notch ligand Dll4 and increased Notch signaling in a process requiring the vasoactive hormone adrenomedullin. Notch signaling also upregulated Dll4 expression, leading to a positive feedback loop sustaining Dll4 expression and Notch signaling. In addition, hypoxia-mediated upregulation of the arterial marker genes Depp, connexin40 (Gja5), Cxcr4, and Hey1 required Notch signaling. In conclusion, the data reveal an intricate interaction between hypoxia and Notch signaling in the control of endothelial cell differentiation, including a hypoxia/adrenomedullin/Dll4 axis that initiates Notch signaling and a requirement for Notch signaling to effectuate hypoxia-mediated induction of the arterial differentiation program.
21.	Li, Fusheng, et al. (author) Dye-sensitized LaFeO3 photocathode for solar-driven H-2 generation 2019 In: Chemical Communications. - : Royal Society of Chemistry. - 1359-7345 .- 1364-548X. ; 55:86, s. 12940-12943 Journal article (peer-reviewed)abstract Mesoporous LaFeO3 was used as a p-type visible-light-absorbing semiconductor (VLAS) substrate for light-driven H-2 generation. The successful modification of LaFeO3 with a molecular dye (P1*) and a molecular hydrogen production catalyst (NiP) paved a novel way to construct DS-PEC photocathodes for solar-driven H-2 generation by using VLASs.
22.	Li, Xiujuan, et al. (author) Embryonic stem cell models in vascular biology 2009 In: Journal of Thrombosis and Haemostasis. - : Elsevier BV. - 1538-7933 .- 1538-7836. ; 7:Suppl. 1, s. 53-56 Research review (peer-reviewed)abstract Embryonic stem cells have become an established tool in vascular biology to study the details of vasculogenesis as well as angiogenesis. There is also a future potential in using embryonic stem cell-derived endothelial cells for therapeutic purposes. It is important to evaluate this model by comparing features of endothelial cells derived from differentiating stem cells and their responsiveness to external stimuli to those of primary endothelial cells and to in vivo models. Through culture of mouse embryonic stem cell we discovered that differentiating stem cells are highly amenable to analyzing biochemical and cell biologic processes that are independent of flow. Endothelial cell function can be studied in the context of mutations or deletions that are embryonically lethal in vivo. Many, if not all, of the features of sprouting angiogenesis in differentiating stem cells closely mimic the in vivo process.
23.	Li, Xiujuan, et al. (author) Lentiviral rescue of vascular endothelial growth factor receptor-2 expression in flk1-/- embryonic stem cells shows early priming of endothelial precursors 2007 In: Stem Cells. - : Oxford University Press (OUP). - 1066-5099 .- 1549-4918. ; 25:12, s. 2987-2995 Journal article (peer-reviewed)abstract The vascular endothelial growth factor ( VEGF) family and its receptors are important for vascular development and maintenance of blood vessels, as well as for angiogenesis, the formation of new vessels. Loss of VEGF receptor-2 (VEGFR-2; designated Flk-1 in mouse) results in arrest of vascular and hematopoietic development in vivo. We used lentiviral transduction to reconstitute VEGFR-2 expression in flk1-/- embryonic stem (ES) cells. VEGF-induced vasculogenesis and sprouting angiogenesis were rescued in transduced ES cultures differentiating in vitro as EBs. Although the transgene was expressed in the pluripotent stem cells and lacked linage restriction during differentiation, the extent of endothelial recruitment was similar to that in wild-type EBs. Reconstitution of VEGFR-2 in flk1-/- ES cells allowed only precommitted precursors to differentiate into functional endothelial cells able to organize into vascular structures. Chimeric EB cultures composed of wild-type ES cells mixed with flk1-/- ES cells or reconstituted VEGFR-2expressing ES cells were created. In the chimeric cultures, flk1-/- endothelial precursors were excluded from wild-type vessel structures, whereas reconstituted VEGFR-2-expressing precursors became integrated together with wild-type endothelial cells to form chimeric vessels. We conclude that maturation of endothelial precursors, as well as organization into vascular structures, requires expression of VEGFR-2.
24.	Li, Xiujuan, et al. (author) Pro-tumoral immune cell alterations in wild type and Shb-deficient mice in response to 4T1 breast carcinomas 2018 In: Oncotarget. - : Impact Journals, LLC. - 1949-2553. ; 9:27, s. 18720-18733 Journal article (peer-reviewed)abstract To assess mechanisms responsible for breast carcinoma metastasis, 4T1 breast carcinomas were grown orthotopically in wild type or Shb knockout mice. Tumor growth, metastasis, vascular characteristics and immune cell properties were analyzed. Absence of Shb did not affect tumor growth although it increased lung metastasis. Shb knockout mouse tumors showed decreased redness and less developed vascular plexa located at the periphery of the tumors. No difference in overall tumor vascular density, leakage or pericyte coverage was noted between the genotypes although the average vessel size was smaller in the knockout. Tumors induced an increase of CD11b+ cells in spleen, lymph node, thymus, bone marrow and blood. Numbers of Shb knockout CD11b/CD8+ cells were decreased in lymph nodes and bone marrow of tumor bearing mice. Mice with tumors had reduced numbers of CD4+ lymphocytes in blood/lymphoid organs, whereas in most of these locations the proportion of CD4+ cells co-expressing FoxP3 was increased, suggesting a relative increase in Treg cells. This finding was reinforced by increased blood interleukin-35 (IL-35) in wild type tumor bearing mice. Shb knockout blood showed in addition an increased proportion of IL-35 expressing Treg cells, supporting the notion that absence of Shb further promotes tumor evasion from immune cell recognition. This could explain the increased number of lung metastases observed under these conditions. In conclusion, 4T1 tumors alter immune cell responses that promote tumor expansion, metastasis and escape from T cell recognition in an Shb dependent manner.
25.	Li, Xiujuan, et al. (author) Suppressed Vascular Leakage and Myocardial Edema Improve Outcome From Myocardial Infarction 2020 In: Frontiers in Physiology. - : Frontiers Media SA. - 1664-042X. ; 11 Journal article (peer-reviewed)abstract Aim: The acute phase of myocardial infarction (MI) is accompanied by edema contributing to tissue damage and disease outcome. Here, we aimed to identify the mechanism whereby vascular endothelial growth factor (VEGF)-A induces myocardial edema in the acute phase of MI to eventually promote development of therapeutics to specifically suppress VEGFA-regulated vascular permeability while preserving collateral vessel formation.Methods and Results: VEGFA regulates vascular permeability and edema by activation of VEGF receptor-2 (VEGFR2), leading to induction of several signaling pathways including the cytoplasmic tyrosine kinase c-Src. The activated c-Src in turn phosphorylates vascular endothelial (VE)-cadherin, leading to dissociation of endothelial adherens junctions. A particular tyrosine at position 949 in mouse VEGFR2 has been shown to be required for activation of c-Src. Wild-type mice and mice with phenylalanine replacing tyrosine (Y) 949 in VEGFR2 (Vegfr2Y949F/Y949F) were challenged with MI through permanent ligation of the left anterior descending coronary artery. The infarct size was similar in wild-type and mutant mice, but left ventricular wall edema and fibrinogen deposition, indicative of vascular leakage, were reduced in the Vegfr2Y949F/Y949F strain. When challenged with large infarcts, the Vegfr2Y949F/Y949F mice survived significantly better than the wild-type strain. Moreover, neutrophil infiltration and levels of myeloperoxidase were low in the infarcted Vegfr2Y949F/Y949F hearts, correlating with improved survival. In vivo tyrosine phosphorylation of VE-cadherin at Y685, implicated in regulation of vascular permeability, was induced by circulating VEGFA in the wild-type but remained at baseline levels in the Vegfr2Y949F/Y949F hearts.Conclusion: Suppression of VEGFA/VEGFR2-regulated vascular permeability leads to diminished edema without affecting vascular density correlating with improved myocardial parameters and survival after MI.
26.	Li, Xiujuan, et al. (author) VEGF receptor signal transduction 2008 In: Angiogenesis. - San Diego, USA : Elsevier. - 9780123743152 ; , s. 261-284 Book chapter (other academic/artistic)abstract Signal transduction by vascular endothelial growth factors (VEGFs) through their cognate VEGF receptor tyrosine kinases follows the consensus scheme for receptor tyrosine kinases. Thus, binding of ligand induces receptor dimerization and activation of the tyrosine kinase through transphosphorylation between receptor molecules, leading to initiation of intracellular signal transduction pathways. Certain signal transduction pathways are shared with most, if not all, receptor tyrosine kinases, whereas some may be unique (e.g., transduced only by VEGF receptors). Indications that such unique signaling pathways may be discerned only when VEGF receptors are expressed in their proper context (i.e., in endothelial cells of microcapillary origin). In this chapter, we describe a number of methods for the study of signal transduction in endothelial cells. We describe how to isolate and examine endothelial cell lines. We also describe the embryoid body model representing vasculogenesis and angiogenesis, the procedure for subcutaneous Matrigel plugs, and, finally, how to construct gene-targeted mouse models. We emphasize the need for validation of in vitro data in more complex models, where endothelial cells reside in their proper three-dimensional context.
27.	Li, Xiujuan, et al. (author) VEGFR2 pY949 signalling regulates adherens junction integrity and metastatic spread 2016 In: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 7 Journal article (peer-reviewed)abstract The specific role of VEGFA-induced permeability and vascular leakage in physiology and pathology has remained unclear. Here we show that VEGFA-induced vascular leakage depends on signalling initiated via the VEGFR2 phosphosite Y949, regulating dynamic c-Src and VE-cadherin phosphorylation. Abolished Y949 signalling in the mouse mutant Vegfr2(Y949F/Y949F) leads to VEGFA-resistant endothelial adherens junctions and a block in molecular extravasation. Vessels in Vegfr2(Y949F/Y949F) mice remain sensitive to inflammatory cytokines, and vascular morphology, blood pressure and flow parameters are normal. Tumour-bearing Vegfr2(Y949F/Y949F) mice display reduced vascular leakage and oedema, improved response to chemotherapy and, importantly, reduced metastatic spread. The inflammatory infiltration in the tumour micro-environment is unaffected. Blocking VEGFA-induced disassembly of endothelial junctions, thereby suppressing tumour oedema and metastatic spread, may be preferable to full vascular suppression in the treatment of certain cancer forms.
28.	Ma, Liang, et al. (author) Room-Temperature Near-Infrared Photodetectors Based on Single Heterojunction Nanowires 2014 In: Nano Letters. - : American Chemical Society (ACS). - 1530-6992 .- 1530-6984. ; 14:2, s. 694-698 Journal article (peer-reviewed)abstract Nanoscale near-infrared photodetectors are attractive for their potential applications in integrated optoelectronic devices. Here we report the synthesis of GaSb/GaInSb p-n heterojunction semiconductor nanowires for the first time through a controllable chemical vapor deposition (CVD) route. Based on these nanowires, room-temperature, high-performance, near-infrared photodetectors were constructed. The fabricated devices show excellent light response in the infrared optical communication region (1.55 mu m), with an external quantum efficiency of 10(4), a responsivity of 10(3) A/W, and a short response time of 2 ms, which shows promising potential applications in integrated photonics and optoelectronics devices or systems.
29.	Nilsson, Ingrid, et al. (author) VEGF receptor 2/-3 heterodimers detected in situ by proximity ligation on angiogenic sprouts 2010 In: EMBO Journal. - : Wiley. - 0261-4189 .- 1460-2075. ; 29:8, s. 1377-1388 Journal article (peer-reviewed)abstract The vascular endothelial growth factors VEGFA and VEGFC are crucial regulators of vascular development. They exert their effects by dimerization and activation of the cognate receptors VEGFR2 and VEGFR3. Here, we have used in situ proximity ligation to detect receptor complexes in intact endothelial cells. We show that both VEGFA and VEGFC potently induce formation of VEGFR2/-3 heterodimers. Receptor heterodimers were found in both developing blood vessels and immature lymphatic structures in embryoid bodies. We present evidence that heterodimers frequently localize to tip cell filopodia. Interestingly, in the presence of VEGFC, heterodimers were enriched in the leading tip cells as compared with trailing stalk cells of growing sprouts. Neutralization of VEGFR3 to prevent heterodimer formation in response to VEGFA decreased the extent of angiogenic sprouting. We conclude that VEGFR2/-3 heterodimers on angiogenic sprouts induced by VEGFA or VEGFC may serve to positively regulate angiogenic sprouting.
30.	Rolny, Charlotte, et al. (author) HRG Inhibits Tumor Growth and Metastasis by Inducing Macrophage Polarization and Vessel Normalization through Downregulation of PIGF 2011 In: Cancer Cell. - : Elsevier BV. - 1535-6108 .- 1878-3686. ; 19:1, s. 31-44 Journal article (peer-reviewed)abstract Polarization of tumor-associated macrophages (TAMs) to a proangiogenic/immune-suppressive (M2-like) phenotype and abnormal, hypoperfused vessels are hallmarks of malignancy, but their molecular basis and interrelationship remains enigmatic. We report that the host-produced histidine-rich glycoprotein (HRG) inhibits tumor growth and metastasis, while improving chemotherapy. By skewing TAM polarization away from the M2- to a tumor-inhibiting M1-like phenotype, HRG promotes antitumor immune responses and vessel normalization, effects known to decrease tumor growth and metastasis and to enhance chemotherapy. Skewing of TAM polarization by HAG relies substantially on downregulation of placental growth factor (PIGF). Besides unveiling an important role for TAM polarization in tumor vessel abnormalization, and its regulation by HRG/PIGF, these findings offer therapeutic opportunities for anticancer and antiangiogenic treatment.
31.	Sáinz-Jaspeado, Miguel, et al. (author) VE-cadherin junction dynamics in initial lymphatic vessels promotes lymph node metastasis 2024 In: Life Science Alliance. - : Life Science Alliance. - 2575-1077. ; 7:3 Journal article (peer-reviewed)abstract The endothelial junction component vascular endothelial (VE)–cadherin governs junctional dynamics in the blood and lymphatic vasculature. Here, we explored how lymphatic junction stability is modulated by elevated VEGFA signaling to facilitate metastasis to sentinel lymph nodes. Zippering of VE-cadherin junctions was established in dermal initial lymphatic vessels after VEGFA injection and in tumor-proximal lymphatics in mice. Shape analysis of pan-cellular VE-cadherin fragments revealed that junctional zippering was accompanied by accumulation of small round-shaped VE-cadherin fragments in the lymphatic endothelium. In mice expressing a mutant VEGFR2 lacking the Y949 phosphosite (Vegfr2Y949F/Y949F) required for activation of Src family kinases, zippering of lymphatic junctions persisted, whereas accumulation of small VE-cadherin fragments was suppressed. Moreover, tumor cell entry into initial lymphatic vessels and subsequent metastatic spread to lymph nodes was reduced in mutant mice compared with WT, after challenge with B16F10 melanoma or EO771 breast cancer. We conclude that VEGFA mediates zippering of VE-cadherin junctions in initial lymphatics. Zippering is accompanied by increased VE-cadherin fragmentation through VEGFA-induced Src kinase activation, correlating with tumor dissemination to sentinel lymph nodes.
32.	Sun, Zuyue, et al. (author) VEGFR2 induces c-Src signaling and vascular permeability in vivo via the adaptor protein TSAd 2012 In: Journal of Experimental Medicine. - : Rockefeller University Press. - 0022-1007 .- 1540-9538. ; 209:7, s. 1363-1377 Journal article (peer-reviewed)abstract Regulation of vascular endothelial (VE) growth factor (VEGF)-induced permeability is critical in physiological and pathological processes. We show that tyrosine phosphorylation of VEGF receptor 2 (VEGFR2) at Y951 facilitates binding of VEGFR2 to the Rous sarcoma (Src) homology 2-domain of T cell-specific adaptor (TSAd), which in turn regulates VEGF-induced activation of the c-Src tyrosine kinase and vascular permeability. c-Src was activated in vivo and in vitro in a VEGF/TSAd-dependent manner, and was regulated via increased phosphorylation at pY418 and reduced phosphorylation at pY527. Tsad silencing blocked VEGF-induced c-Src activation, but did not affect pathways involving phospholipase C gamma, extracellular regulated kinase, and endothelial nitric oxide. VEGF-induced rearrangement of VE-cadherin-positive junctions in endothelial cells isolated from mouse lungs, or in mouse cremaster vessels, was dependent on TSAd expression, and TSAd formed a complex with VE-cadherin, VEGFR2, and c-Src at endothelial junctions. Vessels in tsad(-/-) mice showed undisturbed flow and pressure, but impaired VEGF-induced permeability, as measured by extravasation of Evans blue, dextran, and microspheres in the skin and the trachea. Histamine-induced extravasation was not affected by TSAd deficiency. We conclude that TSAd is required for VEGF-induced, c-Src-mediated regulation of endothelial cell junctions and for vascular permeability.
33.	Testini, Chiara, et al. (author) VEGFR2 pY1212 signaling regulates endothelial cell proliferation and vessel stability Other publication (other academic/artistic)
34.	Tugues, Sonia, et al. (author) Tetraspanin CD63 Promotes Vascular Endothelial Growth Factor Receptor 2-beta 1 Integrin Complex Formation, Thereby Regulating Activation and Downstream Signaling in Endothelial Cells in Vitro and in Vivo 2013 In: Journal of Biological Chemistry. - 0021-9258 .- 1083-351X. ; 288:26, s. 19060-19071 Journal article (peer-reviewed)abstract CD63 is a member of the transmembrane-4 glycoprotein superfamily (tetraspanins) implicated in the regulation of membrane protein trafficking, leukocyte recruitment, and adhesion processes. We have investigated the involvement of CD63 in endothelial cell (EC) signaling downstream of beta 1 integrin and VEGF. We report that silencing of CD63 in primary ECs arrested capillary sprouting and tube formation in vitro because of impaired adhesion and migration of ECs. Mechanistically, CD63 associated with both beta 1 integrin and the main VEGF receptor on ECs, VEGFR2. Our data suggest that CD63 serves to bridge between beta 1 integrin and VEGFR2 because CD63 silencing disrupted VEGFR2-beta 1 integrin complex formation identified using proximity ligation assays. Signaling downstream of beta 1 integrin and VEGFR2 was attenuated in CD63-silenced cells, although their cell surface expression levels remained unaffected. CD63 was furthermore required for efficient internalization of VEGFR2 in response to VEGF. Importantly, systemic delivery of VEGF failed to potently induce VEGFR2 phosphorylation and downstream signaling in CD63-deficient mouse lungs. Taken together, our findings demonstrate a previously unrecognized role for CD63 in coordinated integrin and receptor tyrosine kinase signaling in vitro and in vivo.
35.	Tugues, Sonia, et al. (author) Vascular endothelial growth factors and receptors : Anti-angiogenic therapy in the treatment of cancer 2011 In: Molecular Aspects of Medicine. - : Elsevier BV. - 0098-2997 .- 1872-9452. ; 32:2, s. 88-111 Research review (peer-reviewed)abstract Vascular endothelial growth factors (VEGFs) are critical regulators of vascular and lymphatic function during development, in health and in disease. There are five mammalian VEGF ligands and three VEGF receptor tyrosine kinases. In addition, several VEGF co-receptors that lack intrinsic catalytic activity, but that indirectly modulate the responsiveness to VEGF contribute to the final biological effect. This review describes the molecular features of VEGFs. VEGFRs and co-receptors with focus on their role in the treatment of cancer.
36.	Wu, Xiujuan, et al. (author) Metalloid Te-Doped Fe-Based Catalysts Applied for Electrochemical Water Oxidation 2021 In: CHEMISTRYSELECT. - : Wiley. - 2365-6549. ; 6:24, s. 6154-6158 Journal article (peer-reviewed)abstract Metal telluride nanocatalysts have been widely used in the catalytic reactions. However, there are few examples of electrocatalytic water oxidation with metal telluride as catalysts, especially Fe-based telluride, to the best of our knowledge, has not yet been reported. In this work, the Te-doped Fe-based catalysts (FeTex) with crystalline and amorphous nanosheet structures have been successfully synthesized by chemical vapor deposition (CVD) as well as electrodeposition (ED) on the iron foam (IF), where the latter exhibited more remarkable electrocatalytic performance towards the oxygen evolution reaction (OER) in the alkaline electrolyte, requiring the overpotential (eta) of only 264.4 mV to reach a current density of 10 mA cm(-2) with a Tafel slope of 54.2 mV dec(-1). The electrochemical study confirmed that the residual Te in ED-FeTex does play a role in promoting the catalytic activity for the electrocatalytic water oxidation.
37.	Zhang, Lei, et al. (author) Pleiotrophin promotes vascular abnormalization in glioma and correlates withpoor survival in human astrocytomas Journal article (other academic/artistic)
38.	Zhang, Lei, et al. (author) Pleiotrophin promotes vascular abnormalization in gliomas and correlates with poor survival in patients with astrocytomas 2015 In: Science signaling. - : American Association for the Advancement of Science (AAAS). - 1937-9145 .- 1945-0877. ; 8:406, s. ra125- Journal article (peer-reviewed)abstract Secretion of pleiotrophin by aggressive gliomas triggers the formation of abnormal blood vessels by endothelial cells.
39.	Zhao, Ziqi, et al. (author) Molecular Engineering of Photocathodes based on Polythiophene Organic Semiconductors for Photoelectrochemical Hydrogen Generation 2021 In: ACS Applied Materials and Interfaces. - : American Chemical Society (ACS). - 1944-8244 .- 1944-8252. ; 13:34, s. 40602-40611 Journal article (peer-reviewed)abstract Organic semiconductors provide significant potentials for the construction of photoelectrochemical (PEC) cells for solar hydrogen production because of their highly tunable properties. Herein, on carbon fiber paper (CFP) surface, pyridyl (Py), and 4,4'-bipyridin-1-ium (Py-2(+)) groups were introduced into polythiophene (pTH) semiconductor by electrochemical copolymerization, respectively. After assembly with the Co(dmgBF(2))(2) type catalyst (CoB, dmgBF(2) = difluoroboryldimethylglyoximate), the CoB@Py-2(+)-pTH/CFP photocathode displayed nearly twice the photocurrent enhancement (550 mu A cm(-2) at 0.15 V vs reversible hydrogen electrode, RHE) comparing to that generated by the CoB@Py-pTH/CFP photocathode (290 mu A cm(-2) at 0.15 V vs RHE) for light-driven H-2 generation under AM 1.5 solar illumination. Investigation of the mechanism revealed that the introduction of the positively charged pyridinium groups could improve the intrinsic Co(dmgBF(2))(2) catalyst activity for the H-2 generation reaction. Meanwhile, the positively charged pyridinium groups serve as p-type dopants to increase the semiconductor bulk charge transfer rate and act as electron transfer mediators to promote the interfacial charge transfer kinetics between the catalyst and the pTH-based organic semiconductor.

Skapa referenser, mejla, bekava och länka

Permalink

Träfflista för sökning "WFRF:(Li Xiujuan) "

Refine your search

Year