| 1. |
- Di, Dongmei, et al.
(author)
-
ABCA1 upregulating apolipoproein M expression mediates via the RXR/LXR pathway in HepG2 cells
- 2012
-
In: Biochemical and Biophysical Research Communications. - : Elsevier BV. - 1090-2104 .- 0006-291X. ; 421:1, s. 152-156
-
Journal article (peer-reviewed)abstract
- We have previously reported that liver X receptor (LXR) agonist, TO901317, could significantly inhibit hepatic apolipoprotein M (apoM) expression. It has been reported that TO901317 could activate the ATP-binding cassette transporter A1 (ABCA1) that mediates cholesterol efflux to the lipid-poor apoA1, which is an essential step for the high-density lipoprotein (HDL) formation. It is unknown if ABCA1 may regulate hepatic apoM expression. In the present study, HepG2 cells were cultured with the synthetic LXR agonists, TO901317 or GW3965 in the presence or absence of ABCA1 antagonist, disodium 4,4'-diisothiocyanatostilbene-2,2'-disulfonate (DIDS). The mRNA levels of ABCA1, apoM and liver receptor homolog-1 (LRH-1) determined by the real-time RT-PCR. It demonstrated that both TO901317 and GW3965 could significantly enhance ABCA1 expression, and simultaneously, inhibit LRH1 expression. However, TO901317 alone could significantly inhibit apoM expression, while GW3965 alone did not influence apoM expression. ABCA1 antagonist, DIDS, have no effects on GW3965 induced upregulation of ABCA1 and downregulation of LRH1. However, apoM mRNA level was significantly decreased when the cells cultured with GW3965 together with DIDS. The present study demonstrated that apoM expression could be elevated by ABCA1 via the RXR/LXR pathway and LRH1 does not involve in the regulation of apoM by the activation of ABCA1, although the direct regulative pathway(s) between ABCA1 and apoM gene is still unknown yet. The detailed mechanism needs further investigation. (C) 2012 Elsevier Inc. All rights reserved.
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| 2. |
- Griffiths, Natalie A., et al.
(author)
-
Temporal and Spatial Variation in Peatland Carbon Cycling and Implications for Interpreting Responses of an Ecosystem-Scale Warming Experiment
- 2017
-
In: Soil Science Society of America Journal. - : ACSESS. - 0361-5995 .- 1435-0661. ; 81:6, s. 1668-1688
-
Journal article (peer-reviewed)abstract
- We are conducting a large-scale, long-term climate change response experiment in an ombrotrophic peat bog in Minnesota to evaluate the effects of warming and elevated CO2 on ecosystem processes using empirical and modeling approaches. To better frame future assessments of peatland responses to climate change, we characterized and compared spatial vs. temporal variation in measured C cycle processes and their environmental drivers. We also conducted a sensitivity analysis of a peatland C model to identify how variation in ecosystem parameters contributes to model prediction uncertainty. High spatial variability in C cycle processes resulted in the inability to determine if the bog was a C source or sink, as the 95% confidence interval ranged from a source of 50 g C m(-2) yr(-1) to a sink of 67 g C m(-2) yr(-1). Model sensitivity analysis also identified that spatial variation in tree and shrub photosynthesis, allocation characteristics, and maintenance respiration all contributed to large variations in the pretreatment estimates of net C balance. Variation in ecosystem processes can be more thoroughly characterized if more measurements are collected for parameters that are highly variable over space and time, and especially if those measurements encompass environmental gradients that may be driving the spatial and temporal variation (e.g., hummock vs. hollow microtopographies, and wet vs. dry years). Together, the coupled modeling and empirical approaches indicate that variability in C cycle processes and their drivers must be taken into account when interpreting the significance of experimental warming and elevated CO2 treatments.
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| 3. |
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| 4. |
- Luo, Guanghua, et al.
(author)
-
Palmitic acid suppresses apolipoprotein M gene expression via the pathway of PPARβ/δ in HepG2 cells.
- 2014
-
In: Biochemical and Biophysical Research Communications. - : Elsevier BV. - 1090-2104 .- 0006-291X. ; 445:1, s. 203-207
-
Journal article (peer-reviewed)abstract
- It has been demonstrated that apolipoprotein M (APOM) is a vasculoprotective constituent of high density lipoprotein (HDL), which could be related to the anti-atherosclerotic property of HDL. Investigation of regulation of APOM expression is of important for further exploring its pathophysiological function in vivo. Our previous studies indicated that expression of APOM could be regulated by platelet activating factor (PAF), transforming growth factors (TGF), insulin-like growth factor (IGF), leptin, hyperglycemia and etc., in vivo and/or in vitro. In the present study, we demonstrated that palmitic acid could significantly inhibit APOM gene expression in HepG2 cells. Further study indicated neither PI-3 kinase (PI3K) inhibitor LY294002 nor protein kinase C (PKC) inhibitor GFX could abolish palmitic acid induced down-regulation of APOM expression. In contrast, the peroxisome proliferator-activated receptor beta/delta (PPARβ/δ) antagonist GSK3787 could totally reverse the palmitic acid-induced down-regulation of APOM expression, which clearly demonstrates that down-regulation of APOM expression induced by palmitic acid is mediated via the PPARβ/δ pathway.
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| 5. |
- Luo, Guanghua, et al.
(author)
-
Rosiglitazone Enhances Apolipoprotein M (Apom) Expression in Rat's Liver.
- 2014
-
In: International Journal of Medical Sciences. - : Ivyspring International Publisher. - 1449-1907. ; 11:10, s. 1015-1021
-
Journal article (peer-reviewed)abstract
- Apolipoprotein M (APOM) has been suggested as a vasculoprotective constituent of high density lipoprotein (HDL), which plays a crucial role behind the mechanism of HDL-mediated anti-atherosclerosis. Previous studies demonstrated that insulin resistance could associate with decreased APOM expressions. In agreement with our previous reports, here, we further confirmed that the insulin sensitivity was also reduced in rats treated with high concentrations of glucose; such effect could be reversed by administration of rosiglitazone, a peroxisome proliferator-activated receptor-γ (PPARγ). The present study shows that Apom expression is significantly affected by either rosiglitazone or hyperglycemia alone without cross interaction with each other, which indicates that the pathway of Apom expression regulating by hyperglycemia might be differed from that by rosiglitazone. Further study indicated that hyperglycemia could significantly inhibit mRNA levels of Lxrb (P=0.0002), small heterodimer partner 1 (Shp1) (P<0.0001), liver receptor homologue-1 (Lrh1) (P=0.0012), ATP-binding cassette transporter 1 (Abca1) (P=0.0012) and Pparb/d (P=0.0043). Two-way ANOVA analysis demonstrated that the interactions between rosiglitazone and infusion of 25% glucose solution on Shp1 (P=0.0054) and Abca1 (4E, P=0.0004) mRNA expression was statistically significant. It is concluded that rosiglitazone could increase Apom expression, of which the detailed mechanism needs to be further investigated. The downregulation of Apom by hyperglycemia might be mainly through decreasing expression of Pparg and followed by inhibiting Lxrb in rats.
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| 6. |
- Metcalfe, Daniel, et al.
(author)
-
Informing climate models with rapid chamber measurements of forest carbon uptake
- 2017
-
In: Global Change Biology. - : Wiley. - 1354-1013 .- 1365-2486. ; 23:5, s. 2130-2139
-
Journal article (peer-reviewed)abstract
- Models predicting ecosystem carbon dioxide (CO2) exchange under future climate change rely on relatively few real-world tests of their assumptions and outputs. Here, we demonstrate a rapid and cost-effective method to estimateCO2exchange from intact vegetation patches under varying atmospheric CO2concentrations.We find that net ecosys-tem CO2uptake (NEE) in a boreal forest rose linearly by 4.7 0.2% of the current ambient rate for every 10 ppmCO2increase, with no detectable influence of foliar biomass, season, or nitrogen (N) fertilization. The lack of any clearshort-term NEE response to fertilization in such an N-limited system is inconsistent with the instantaneous downreg-ulation of photosynthesis formalized in many global models. Incorporating an alternative mechanism with consider-able empirical support – diversion of excess carbon to storage compounds – into an existing earth system modelbrings the model output into closer agreement with our field measurements. A global simulation incorporating thismodified model reduces a long-standing mismatch between the modeled and observed seasonal amplitude of atmo-spheric CO2. Wider application of this chamber approach would provide critical data needed to further improvemodeled projections of biosphere–atmosphere CO2exchange in a changing climate.
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| 7. |
- Piao, Shilong, et al.
(author)
-
Evidence for a weakening relationship between interannual temperature variability and northern vegetation activity.
- 2014
-
In: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 5
-
Journal article (peer-reviewed)abstract
- Satellite-derived Normalized Difference Vegetation Index (NDVI), a proxy of vegetation productivity, is known to be correlated with temperature in northern ecosystems. This relationship, however, may change over time following alternations in other environmental factors. Here we show that above 30°N, the strength of the relationship between the interannual variability of growing season NDVI and temperature (partial correlation coefficient RNDVI-GT) declined substantially between 1982 and 2011. This decrease in RNDVI-GT is mainly observed in temperate and arctic ecosystems, and is also partly reproduced by process-based ecosystem model results. In the temperate ecosystem, the decrease in RNDVI-GT coincides with an increase in drought. In the arctic ecosystem, it may be related to a nonlinear response of photosynthesis to temperature, increase of hot extreme days and shrub expansion over grass-dominated tundra. Our results caution the use of results from interannual time scales to constrain the decadal response of plants to ongoing warming.
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| 8. |
- Qiu, Xiaoying, et al.
(author)
-
A programmable baseband processor for massive MIMO uplink multi-user detection
- 2016
-
In: Proceedings - 2015 IEEE 11th International Conference on ASIC, ASICON 2015. - 9781479984831
-
Conference paper (peer-reviewed)abstract
- Massive MIMO is a promising technology for the coming 5G wireless systems. In this paper, a programmable baseband processor specifically designed for uplink symbol detection targeting massive MIMO is presented with a novel matrix inversion method proposed to obtain more precise and efficient computation. Including a microcode controlled channel preprocessing unit and a pipelined detection unit, the detector is flexible enough to adaptively support both linear and nonlinear detection algorithms.
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| 9. |
- Shi, Yuanping, et al.
(author)
-
Comprehensive lipidomics in apoM−/− mice reveals an overall state of metabolic distress and attenuated hepatic lipid secretion into the circulation
- 2020
-
In: Journal of Genetics and Genomics. - : Elsevier BV. - 1673-8527. ; 47:9, s. 523-534
-
Journal article (peer-reviewed)abstract
- Apolipoprotein M (apoM) participates in both high-density lipoprotein and cholesterol metabolism. Little is known about how apoM affects lipid composition of the liver and serum. In this study, we systemically investigated the effects of apoM on liver and plasma lipidomes and how apoM participates in lipid cycling, via apoM knockout in mice and the human SMMC-7721 cell line. We used integrated mass spectrometry–based lipidomics approaches to semiquantify more than 600 lipid species from various lipid classes, which include free fatty acids, glycerolipids, phospholipids, sphingolipids, glycosphingolipids, cholesterol, and cholesteryl esters (CEs), in apoM−/− mouse. Hepatic accumulation of neutral lipids, including CEs, triacylglycerols, and diacylglycerols, was observed in apoM−/− mice; while serum lipidomic analyses showed that, in contrast to the liver, the overall levels of CEs and saturated/monounsaturated fatty acids were markedly diminished. Furthermore, the level of ApoB-100 was dramatically increased in the liver, whereas significant reductions in both ApoB-100 and low-density lipoprotein (LDL) cholesterol were observed in the serum of apoM−/− mice, which indicated attenuated hepatic LDL secretion into the circulation. Lipid profiles and proinflammatory cytokine levels indicated that apoM−/− leads to hepatic steatosis and an overall state of metabolic distress. Taken together, these results revealed that apoM knockout leads to hepatic steatosis, impaired lipid secretion, and an overall state of metabolic distress.
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| 10. |
- Shi, Yuanping, et al.
(author)
-
Increased expression levels of inflammatory cytokines and adhesion molecules in lipopolysaccharide‑induced acute inflammatory apoM‑/‑ mice
- 2020
-
In: Molecular Medicine Reports. - : Spandidos Publications. - 1791-2997 .- 1791-3004. ; 22:4, s. 3117-3126
-
Journal article (peer-reviewed)abstract
- apolipoproteinM(apoM)mayserveaprotectiverole inthedevelopmentofinflammation.Nuclearfactor‑κB(nF-κB) and its downstream factors (including a number of inflammatory cytokines and adhesion molecules) are essential for the regulation of inflammatory processes. In the present study, the importance of apoM in lipopolysaccharide (LPS)‑induced acute inflammation and its potential underlying mechanisms, were investigated using an apoM‑knockout mouse model. The levels of inducible nitric oxide synthase (iNOS), NF‑κB, interleukin (IL)‑1β, intercellular adhesion molecule 1 (ICAM‑1) and vascular cell adhesion protein 1 (VCAM‑1) were detected using reverse transcription‑quantitative PCR and western blotting. The serum levels of IL‑6 and IL‑10 were detected using Luminex technology. The results demonstrated that the protein levels of inoS, nF-κB, il-1β, ICAM‑1 and VCAM‑1 were significantly increased in apoM-/- mice compared with those in apoM+/+ mice. In addition, two‑way ANOVA revealed that the interaction between apoM and LPS had a statistically significant effect on a number of factors, including the mRNA expression levels of hepatic iNOS, NF‑κB, il-1β, icaM-1 and VCAM‑1. Notably, the effects of apoM and 10 mg/kg LPS on the levels of IL‑6 and IL‑10 were the opposite of those induced by 5 mg/kg LPS, which could be associated with the dual anti‑ and pro‑inflammatory effects of IL‑6 and IL‑10. Collectively, the results of the present study revealed that apoM is an important regulator of inflammatory cytokine and adhesion molecule production in LPS‑induced inflammation, which may consequently be associated with the severity of inflammation. These findings indicated that the anti‑inflammatory effects of apoM may partly result from the inhibition of the nF-κB pathway.
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| 11. |
- Tu, Tieyao, et al.
(author)
-
Biphyly of the genus Wendlandia and establishment of a new tribe Clavistigmeae and a new genus Clavistigma of Rubiaceae from Asia
- 2024
-
In: Biological Diversity. - 2994-4139. ; , s. 1-17
-
Journal article (peer-reviewed)abstract
- Wendlandia, as currently circumscribed, is a genus of Rubiaceae comprising about 90 species mainly in tropical and subtropical Asia. By sampling species from all four series (Clavigerae, Euexsertae, Montigenae, Subinclusae) and all tribes in the subfamily Dialypetalanthoideae, we examined the monophyly of Wendlandia based on phylogenetic reconstruction using the nuclear ribosomal internal transcribed spacer and four plastid DNA regions. Wendlandia was resolved as biphyletic, consisting of two distantly related lineages that correspond to the monotypic series Clavigerae (Wendlandia pendula), sister to the Chinese endemic genus Trailliaedoxa, and a clade containing the remainder sampled members of Wendlandia. Based on the isolated phylogenetic position of W. pendula and its unique morphological characteristics compared to the recognized tribes of the Vanguerieae alliance, we herein erect a new monotypic genus, Clavistigma, and a new tribe, Clavistigmeae to accommodate the unique species. The secondary pollen presentation and the unique seed morphology were firstly described for the species. The divergence time between Clavistigma and Trailliaedoxa was dated back to 13.8 mya, coinciding with the climate change in northwestern Yunnan driven by the uplift Tibet Plateau and the river incision in the Hengduan Mountains during the Miocene and Late Pliocene.
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| 12. |
- Wei, Jiang, et al.
(author)
-
Estrogen upregulates hepatic apolipoprotein M expression via the estrogen receptor
- 2011
-
In: Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids. - : Elsevier BV. - 1388-1981. ; 1811:12, s. 1146-1151
-
Journal article (peer-reviewed)abstract
- Apolipoprotein M (apoM) is present predominantly in high-density lipoprotein (HDL) in human plasma, thus possibly involved in the regulation of HDL metabolism and the process of atherosclerosis. Although estrogen replacement therapy increases serum levels of apoAl and HDL, it does not seem to reduce the cardiovascular risk in postmenopausal women. Therefore, we investigated the effects of estrogen on apoM expression in vitro and in vivo. HepG2 cells were incubated with different concentrations of estrogen with or without the estrogen receptor antagonist, fulvestrant, and apoM expression in the cells was determined. Hepatic apoM expression and serum levels of apoM were also determined in normal and in ovariectomized rats treated with either placebo or estradiol benzoate, using sham operated rats as controls. Estrogen significantly increased mRNA levels of apoM and apoAl in HepG2 cell cultures in a dose- and time-dependent manner; the upregulation of both apolipoproteins was fully abolished by addition of estrogen receptor antagonist In normal rats, estrogen treatment led to an increase in plasma lipid levels including HDL cholesterol, a marked upregulation of apoM mRNA and a significant increase in serum levels of apoM. The same pattern of regulation was found in ovariectomized rats treated with estrogen. Thus, estrogen upregulates apoM expression both in vivo and in vitro by mechanism(s) involving the estrogen receptor. (C) 2011 Elsevier B.V. All rights reserved.
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| 13. |
- Xue, Xiaoyin, et al.
(author)
-
Enhanced Storage and Interface Structure Stability of NCM811 Cathodes for Lithium-Ion Batteries by Hydrophobic Fluoroalkylsilanes Modification
- 2022
-
In: ENERGY TECHNOLOGY. - : Wiley-VCH Verlagsgesellschaft. - 2194-4288 .- 2194-4296. ; 10:4
-
Journal article (peer-reviewed)abstract
- The nickel-rich ternary-layered oxide LiNixCoyMn(1-x-y)O2 (NCM) cathode exhibits high reversible capacity and low cost; however, severe capacity fade and aggravated air degradation prohibit its widespread commercialization. Herein, the hydrophobic fluoroalkylsilane-modified NCM811 cathode materials are reported. To better understand the effects of electrochemical properties of lithium-ion batteries, a variety of characterization techniques and electrochemical methods are utilized to study the surface chemistry at the cathode/electrolyte interphase. The hydrophobic fluoroalkylsilanes-grafted NCM811 cathode materials suppress the formation of residual lithium even after 30 days in humid air. The fluoroalkylsilanes layer can also provide chemical stabilization to the NCM811 cathode materials by anchoring transition metals (TM) and suppressing TM dissolution during long immersion times in electrolytes. Moreover, the degree of improvement depends on the structure of the fluoroalkylsilanes, such as the number of F groups and the length of carbon chains. As a result, FAS17-modified NCM811 cathode materials after 30-day humid air exposure (humidity 70%) exhibit the greatest overall capacity retention of 74.2% after 200 charge/discharge cycles.
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| 14. |
- Zhang, Xiaoying, et al.
(author)
-
Efficiency Roll-Off in Light-Emitting Electrochemical Cells
- 2024
-
In: Advanced Materials. - : John Wiley and Sons Inc. - 0935-9648 .- 1521-4095. ; 36:15
-
Journal article (peer-reviewed)abstract
- Understanding “efficiency roll-off” (i.e., the drop in emission efficiency with increasing current) is critical if efficient and bright emissive technologies are to be rationally designed. Emerging light-emitting electrochemical cells (LECs) can be cost- and energy-efficiently fabricated by ambient-air printing by virtue of the in situ formation of a p-n junction doping structure. However, this in situ doping transformation renders a meaningful efficiency analysis challenging. Herein, a method for separation and quantification of major LEC loss factors, notably the outcoupling efficiency and exciton quenching, is presented. Specifically, the position of the emissive p-n junction in common singlet-exciton emitting LECs is measured to shift markedly with increasing current, and the influence of this shift on the outcoupling efficiency is quantified. It is further verified that the LEC-characteristic high electrochemical-doping concentration renders singlet-polaron quenching (SPQ) significant already at low drive current density, but also that SPQ increases super-linearly with increasing current, because of increasing polaron density in the p-n junction region. This results in that SPQ dominates singlet-singlet quenching for relevant current densities, and significantly contributes to the efficiency roll-off. This method for deciphering the LEC efficiency roll-off can contribute to a rational realization of all-printed LEC devices that are efficient at highluminance.
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| 15. |
- Zhang, Xiaoying, et al.
(author)
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IL-6 Regulates MMP-10 Expression via JAK2/STAT3 Signaling Pathway in a Human Lung Adenocarcinoma Cell Line
- 2009
-
In: Anticancer research. - 1791-7530. ; 29:11, s. 4497-4501
-
Journal article (peer-reviewed)abstract
- We previously reported that matrix metalloproteinase (MMP)-10 mRNA levels were significantly lower in tumor tissues than in adjacent normal tissues in human non-small cell lung cancer (NSCLC), whereas protein levels of MMP-10 were higher in the tumor tissues than the adjacent tissues. The mechanism of this divergence is still unknown. In the present stud), the role of Janus kinase 2/signal transducers and activators of transcription 3 (JAK2/STAT3) on interleukin (IL)-6 mediated regulation of MMP-10 expression was investigated in a human lung adenocarcinoma cell line (A549 cells) and the molecular regulatory mechanism of MMP-10 expression was explored. A549 cells were stimulated by different concentrations of IL-6 with or without AG490, a specific JAK2 inhibitor. It was demonstrated that IL-6 moderately reduced the MMP-10 mRNA levels, whereas it significantly enhanced the MMP-10 protein mass in the A549 cells. This phenomenon mimicked the divergence of mRNA level and protein mass of MMP-10 in human NSCLC. Moreover, the present study indicated that IL-6 regulation of MMP-10 expression was via the JAK2/STAT3 pathway. STAT3 mRNA levels were significantly increased when the cells were treated with IL-6, whereas when AG490 (50 mu M) was added to the cell cultures, IL-6-induced increase of STAT3 mRNA levels was abolished. Meanwhile, AG490 blocked the IL-6-induced inhibition of MMP-10 mRNA as well as blocking the IL-6-induced increase of MMP-10 protein mass in the A549 cells. Neither IL-6 nor AG490 influenced JAK2 mRNA levels in the A549 cell cultures. It is concluded that the JAK2/STAT3 pathway is involved in the IL-6-mediated regulation of MMP-10, and IL-6 can moderately reduce MMP-10 mRNA levels and strongly increase MMP-10 protein mass in human lung adenocarcinoma A549 cells. Contrasting effects of IL-6 on MMP-10 mRNA level and protein concentration in A549 cells may partially explain the divergence of MMP-10 mRNA level and protein mass in human NSCLC.
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| 16. |
- Zheng, Lu, et al.
(author)
-
Decreased activities of apolipoprotein m promoter are associated with the susceptibility to coronary artery diseases.
- 2014
-
In: International Journal of Medical Sciences. - : Ivyspring International Publisher. - 1449-1907. ; 11:4, s. 365-372
-
Journal article (peer-reviewed)abstract
- The present study investigated the correlation among genetic polymorphisms of the proximal promoter region of apolipoprotein M (apoM) gene, the polymorphisms in relation to apoM expressions and the susceptibility to coronary artery diseases (CAD) in a Han Chinese population. Four common polymorphic sites, i.e., T-1628G, C-1065A, T-855C and T-778C, were confirmed, and a new deletion mutation C-724del was found, in 206 CAD patients and 209 non-CAD patients using direct DNA sequencing analyses. Occurrences of alleles T-1628G, T-855C and C-724del were significantly higher in CAD patients compared to non-CAD patients. Moreover we examined all these polymorphisms in relation to apoM expression by applying luciferase reporter assay. It demonstrated that constructs -855C and 724del showed obvious decreased luciferase activities, i.e., (0.93±0.15 vs. 2.11±0.15; P=0.012) and (1.13±0.25 vs. 2.11±0.15; P=0.009) respectively, which indicates these two polymorphisms could confer decreased apoM expressions. Meanwhile the occurrences of these two SNP were also significantly higher in the CAD patients than in non-CAD patients. It is therefore reasonable to speculate that down-regulated apoM expressions in relation to these polymorphisms may affect HDL and cholesterol metabolism in vivo and further influence the susceptibility to CAD, although the underlying mechanisms need further investigation.
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| 17. |
- Zheng, Lu, et al.
(author)
-
Intralipid decreases apolipoprotein m levels and insulin sensitivity in rats.
- 2014
-
In: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 9:8
-
Journal article (peer-reviewed)abstract
- Apolipoprotein M (ApoM) is a constituent of high-density lipoproteins (HDL). It plays a crucial role in HDL-mediated reverse cholesterol transport. Insulin resistance is associated with decreased ApoM levels.
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| 18. |
- Zhu, Chunhua, et al.
(author)
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TO901317 regulating apolipoprotein M expression mediates via the farnesoid X receptor pathway in Caco-2 cells
- 2011
-
In: Lipids in Health and Disease. - 1476-511X. ; 10
-
Journal article (peer-reviewed)abstract
- Background: Apolipoprotein M (apoM) may have potential antiatherosclerotic properties. It has been reported that apoM expression could be regulated by many intracellar and extracellar factors. In the present study we further investigated regulation of apoM expression in Caco-2 cells stimulated by a liver X receptor (LXR) agonist, TO901317. Materials and methods: Caco-2 cells were cultured in the presence of either TO901317, farnesoid X receptor (FXR) antagonist guggulsterone or TO901317 together with guggulsterone at different concentrations for 24 hrs. The mRNA levels of ATP-binding cassette transporter A1 (ABCA1), apoA1, apoM, liver receptor homologue-1 (LRH-1) and short heterodimer partner 1 (SHP1) were determined by real-time RT-PCR. Results: When Caco-2 cell cultured with TO901317 alone, the mRNA levels of ABCA1, apoA1, apoM, LRH-1 and SHP1 were significantly increased with dose-dependent manners (p < 0.05), whereas when the cells cultured with guggulsterone alone, the mRNA levels of apoM, SHP1 and LRH-1 (p < 0.05) were strongly inhibited. Moreover, guggulsterone could abolish the TO901317 enhanced mRNA levels of apoA1 apoM, SHP1 and LRH-1. Conclusion: The present study demonstrated that LXR agonist TO901317 induced apoM expression in Caco-2 cells might be mediated via the LXR/FXR pathway.
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