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Träfflista för sökning "WFRF:(Cao YH) srt2:(2010-2014)"

Sökning: WFRF:(Cao YH) > (2010-2014)

  • Resultat 1-10 av 18
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  • Cao, RH, et al. (författare)
  • VEGFR1-mediated pericyte ablation links VEGF and PlGF to cancer-associated retinopathy
  • 2010
  • Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 1091-6490. ; 107:2, s. 856-861
  • Tidskriftsartikel (refereegranskat)abstract
    • VEGF coordinates complex regulation of cellular regeneration and interactions between endothelial and perivascular cells; dysfunction of the VEGF signaling system leads to retinopathy. Here, we show that systemic delivery of VEGF and placental growth factor (PlGF) by protein implantation, tumors, and adenoviral vectors ablates pericytes from the mature retinal vasculature through the VEGF receptor 1 (VEGFR1)-mediated signaling pathway, leading to increased vascular leakage. In contrast, we demonstrate VEGF receptor 2 (VEGFR2) is primarily expressed in nonvascular photoreceptors and ganglion cells. Moreover, blockade of VEGFR1 but not VEGFR2 significantly restores pericyte saturation in mature retinal vessels. Our findings link VEGF and PlGF to cancer-associated retinopathy, reveal the molecular mechanisms of VEGFR1 ligand-mediated retinopathy, and define VEGFR1 as an important target of antiangiogenic therapy for treatment of retinopathy.
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  • Wong, HLX, et al. (författare)
  • When MT1-MMP meets ADAMs
  • 2012
  • Ingår i: Cell cycle (Georgetown, Tex.). - : Informa UK Limited. - 1551-4005 .- 1538-4101. ; 11:15, s. 2793-2798
  • Tidskriftsartikel (refereegranskat)
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  • Zhang, C, et al. (författare)
  • Angiotensin-converting enzyme 2 attenuates atherosclerotic lesions by targeting vascular cells
  • 2010
  • Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 1091-6490. ; 107:36, s. 15886-15891
  • Tidskriftsartikel (refereegranskat)abstract
    • Angiotensin-converting enzyme 2 (ACE2) is a newly discovered homolog of ACE whose actions oppose those of angiotensin II (AngII). However, the underlying mechanisms by which ACE2 effectively suppresses early atherosclerotic lesions remain poorly understood. Here, we show, both in vitro and in vivo, that ACE2 inhibited the development of early atherosclerotic lesions by suppressing the growth of vascular smooth muscle cells (VSMCs) and improving endothelial function. In a relatively large cohort animal study (66 rabbits), aortic segments transfected by Ad-ACE2 showed significantly attenuated fatty streak formation, neointimal macrophage infiltration, and alleviation of impaired endothelial function. Segments also showed decreased expression of monocyte chemoattractant protein 1, lectin-like oxidized low-density lipoprotein receptor 1, and proliferating cell nuclear antigen, which led to the delayed onset of atherosclerotic lesions. At the cellular level, ACE2 significantly modulated AngII-induced growth and migration in human umbilical vein endothelial cells and VSMCs. The antiatherosclerotic effect of ACE2 involved down-regulation of the ERK-p38, JAK-STAT, and AngII-ROS-NF-κB signaling pathways and up-regulation of the PI3K-Akt pathway. These findings revealed the molecular mechanisms of the antiatherosclerotic activity of ACE2 and suggested that modulation of ACE2 could offer a therapeutic option for treating atherosclerosis.
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  • Cao, YH, et al. (författare)
  • Optimizing the delivery of cancer drugs that block angiogenesis
  • 2010
  • Ingår i: Science translational medicine. - : American Association for the Advancement of Science (AAAS). - 1946-6242 .- 1946-6234. ; 2:15, s. 15ps3-
  • Tidskriftsartikel (refereegranskat)abstract
    • Optimal delivery systems for antiangiogenic drugs must be developed to maximize clinical benefits and minimize adverse effects in cancer patients.
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  • Resultat 1-10 av 18

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