| 1. |
- Luo, Guanghua, et al.
(author)
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Palmitic acid suppresses apolipoprotein M gene expression via the pathway of PPARβ/δ in HepG2 cells.
- 2014
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In: Biochemical and Biophysical Research Communications. - : Elsevier BV. - 1090-2104 .- 0006-291X. ; 445:1, s. 203-207
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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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| 2. |
- Luo, Guanghua, et al.
(author)
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Rosiglitazone Enhances Apolipoprotein M (Apom) Expression in Rat's Liver.
- 2014
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In: International Journal of Medical Sciences. - : Ivyspring International Publisher. - 1449-1907. ; 11:10, s. 1015-1021
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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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| 3. |
- Shi, Yuanping, et al.
(author)
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Expression of Zinc Finger 23 Gene in Human Hepatocellular Carcinoma
- 2011
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In: Anticancer research. - 1791-7530. ; 31:10, s. 3595-3599
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Journal article (peer-reviewed)abstract
- The aim of this study was to investigate the relationship between human zinc finger 23 (ZNF23) expression and clinico-pathological characteristics in patients suffering from hepatocellular carcinoma (HCC), and to investigate ZNF23 expression in relation to cell apoptosis. Patients and Methods: Thirty-seven HCC samples were collected and ZFP23 mRNA levels were determined by real-time reverse transcription-polymerase chain reaction (RTPCR). Correlation between ZNF23 expression and patients' clinical characteristics was analyzed. For determining the effect of ZNF23 on cell apoptosis, HepG2 cells were exposed to cisplatin at different concentrations and ZNF23 mRNA assayed. Results: Median relative mRNA levels of ZNF23 mRNA in HCC tissues and adjacent tissues were 8.84 (3.59-15.05) and 22.20 (13.85-42.90), respectively (U=259.5, p<0.01). Median mRNA levels of ZNF23 in patients with Edmondson stage I+II disease [12.80 (4.80-19.50)] were much higher than those of patients with stage III+IV disease [5.01 (2.88-11.68), U=99.00, p<0.05]. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay demonstrated that cisplatin significantly inhibited cell proliferation of HepG2 cells in a dose-dependent manner, which was positively correlated to cell apoptosis (F=27.89, p<0.01), and in response to increasing cisplatin concentrations, ZNF23 mRNA levels increased in the cells. Conclusion: Cisplatin-induced apoptotic effect in HepG2 cells may be mediated via the up-regulation of ZNF23, which suggests that the ZNF23 gene could play an important role in the development of hepatocellular carcinoma.
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| 4. |
- Wang, Zhigang, et al.
(author)
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Decreased Splenic CD4(+) T-Lymphocytes in Apolipoprotein M Gene Deficient Mice
- 2015
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In: BioMed Research International. - : Hindawi Limited. - 2314-6133 .- 2314-6141.
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Journal article (peer-reviewed)abstract
- Spleen T-lymphocytes, especially CD4(+) T-cells, have been demonstrated to be involved in broad immunomodulation and host-defense activity in vivo. Apolipoprotein M gene (apoM) may have an important role in the regulation of immunoprocess and inflammation, which could be hypothesized to the apoM containing sphingosine-1-phosphate (S1P). In the present study we demonstrate that the splenic CD4(+) T-lymphocytes were obviously decreased in the apoM gene deficient (apoM(-/-)) mice compared to the wild type (apoM(+/+)). Moreover, these mice were treated with lipopolysaccharide (LPS) and it was found that even more pronounced decreasing CD4(+) T-lymphocytes occurred in the spleen compared to the apoM(+/+) mice. The similar phenomena were found in the ratio of CD4(+)/CD8(+) T-lymphocytes. After administration of LPS, the hepatic mRNA levels of tumor necrosis factor-alpha (TNF-alpha) and monocyte chemotactic protein-1 (MCP-1) were markedly increased; however, there were no statistical differences observed between apoM(+/+) mice and apoM(-/-) mice. The present study demonstrated that apoM might facilitate the maintenance of CD4(+) T-lymphocytes or could modify the T-lymphocytes subgroups in murine spleen, which may further explore the importance of apoM in the regulation of the host immunomodulation, although the detailed mechanism needs continuing investigation.
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| 5. |
- Wei, Jiang, et al.
(author)
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Estrogen upregulates hepatic apolipoprotein M expression via the estrogen receptor
- 2011
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In: Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids. - : Elsevier BV. - 1388-1981. ; 1811:12, s. 1146-1151
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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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| 6. |
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| 7. |
- Zheng, Lu, et al.
(author)
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Intralipid decreases apolipoprotein m levels and insulin sensitivity in rats.
- 2014
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In: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 9:8
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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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| 8. |
- Zhu, Yifei, et al.
(author)
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Apolipoprotein M promotes proliferation and invasion in non-small cell lung cancers via upregulating S1PR1 and activating the ERK1/2 and PI3K/AKT signaling pathways
- 2018
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In: Biochemical and Biophysical Research Communications. - : Elsevier BV. - 0006-291X. ; 501:2, s. 520-526
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Journal article (peer-reviewed)abstract
- Apolipoprotein M (ApoM) is a sphingosine 1-phosphate (S1P) carrier involved in the regulation of S1P. Signaling pathways involving sphingosine kinases (SphKs) and S1P-S1P receptors (S1PRs) play important roles in the oncogenesis of multiple cancers including non-small cell lung cancer (NSCLC). In the present study we have clarified the potential roles of ApoM on the oncogenesis process of NSCLC cells. We detected the ApoM expression in NSCLC tissues and further analyzed its clinical significance. Moreover, we determined effects of ApoM overexpression on tumor cellular behaviours of NSCLC in vitro and in vivo. Our results demonstrated that ApoM protein mass were clearly higher in the NSCLC tissues than in non-NSCLS tissues. Overexpression of ApoM could promote NSCLC cell proliferation and invasion in vitro and tumor growth in vivo, which might be via upregulating S1PR1 and activating the ERK1/2 and PI3K/AKT signaling pathways. It is concluded that up-regulation of ApoM in NSCLC might be associated with the tumor induced inflammation and tumor microenvironment as well as promoting oncogenesis of NSCLC. Further study needs to elucidate the underlying mechanisms.
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