| 1. |
- Di, Dongmei, et al.
(författare)
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ABCA1 upregulating apolipoproein M expression mediates via the RXR/LXR pathway in HepG2 cells
- 2012
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Ingår i: Biochemical and Biophysical Research Communications. - : Elsevier BV. - 1090-2104 .- 0006-291X. ; 421:1, s. 152-156
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Tidskriftsartikel (refereegranskat)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. |
- He, X, et al.
(författare)
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Short-term administration of ACTH improves plasma lipid profile and renal function in kidney transplant patients
- 2006
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Ingår i: Transplantation Proceedings. - : Elsevier BV. - 0041-1345. ; 38:5, s. 1371-1374
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Tidskriftsartikel (refereegranskat)abstract
- The present study investigated effects of short-term administration of adrenocorticotrophic hormone (ACTH) on blood lipid profile and renal function in kidney transplant patients. Six patients who had kidney transplantations 2 to 10 years earlier received ACTH intramuscularly (1 mg/d) for 4 days. We analyzed serum levels of lipids, lipoproteins, apolipoproteins, blood creatinine, and other parameters. Short-term ACTH treatment significantly decreased serum apolipoprotein B and apolipoprotein AI, whereas it significantly increased plasma high-density lipoproteins (HDL). Interestingly, creatinine level moderately decreased and creatinine clearances moderately increased among five of six patients. Hepatic function and serum concentration of cyclosporine did not change. There were no serious side effects during ACTH treatment. It was concluded that ACTH treatment had beneficial effects on serum lipoprotein profile, potentially improving renal function in kidney transplant patients. Further observations are needed to confirm these effects.
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| 3. |
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| 4. |
- Jiang, Jingting, et al.
(författare)
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Clinical Evaluation of Serum Alpha-Fetoprotein-IgM Immune Complexes on the Diagnosis of Primary Hepatocellular Carcinoma
- 2009
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Ingår i: Journal of Clinical Laboratory Analysis. - : Wiley. - 1098-2825 .- 0887-8013. ; 23:4, s. 213-218
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Tidskriftsartikel (refereegranskat)abstract
- We evaluated clinical significance of serum alpha-fetoprotein (AFP)-IgM immune complexes, in comparison with free AFP, on the diagnosis of primary hepatocellular carcinoma (HCC). Serum levels of AFP-IgM immune complexes and free AFP were determined by the ELISA method and electrochemiluminescence, respectively, in 103 healthy controls, 74 patients suffering from primary HCC, 27 patients suffering from liver cirrhosis, and 63 patients suffering from chronic hepatitis. The best cut-off value of AFP-IgM and free AFP for diagnosis of primary HCC were 300 AU/mL and 10 mu g/L respectively, according to the area under the curve (AUC) in this study. The sensitivity of AFP-IgM and free AFP were 64.9 and 79.7%, and the specificity were 75.6 and 80.3%, respectively, when all cases of primary HCC were analyzed, and the AUC of free AFP was larger than that of AFP-IgM (0.85 vs. 0.72, Z = 3.21). However, in case of primary HCC at early stages (stages I and II) were analyzed, the AUC of AFP-IgM was larger than that of free AFP (0.91 vs. 0.82, Z = 1.73), which demonstrated that the sensitivity of AFP-IgM and free AFP were 94.4 and 72.2%, and the specificity were 81.9 and 79.9%, respectively. When both AFP-IgM and free AFP were positive, the specificity of diagnosis of primary HCC was 89.1%, and the efficacy was 79.0%. It is concluded that either sensitivity or specificity of serum level of AFP-IgM immune complexes was higher than that of free AFP in the diagnosis of primary HCC at early stages. As there was false positive AFP-IgM existed in the patients suffering from cirrhosis and chronic hepatitis, the combination of free AFP and AFP-IgM could significantly increase specificity and decrease false negative and/or false positive in the primary HCC at early stages. J. Clin. Lab. Anal. 23:213-218, 2009. (C) 2009 Wiley-Liss, Inc.
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| 5. |
- Jiang, Jingting, et al.
(författare)
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Influence of liver cancer on lipid and lipoprotein metabolism
- 2006
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Ingår i: Lipids in Health and Disease. - 1476-511X. ; 5
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Forskningsöversikt (refereegranskat)abstract
- Liver plays a key role in the metabolism of plasma apolipoproteins, endogenous lipids and lipoproteins. Hepatocellular carcinoma (HCC) is one of the most common fatal malignant tumors in China and in other Southeast Asian countries. This has been attributed to the high incidence of hepatitis B infection. Hepatitis B proteins, such as the hepatitis B X protein (HBx) that is large hepatitis B surface protein could regulate transcription of many candidate genes for liver carcinogenesis. It has known that patients who suffered from acute hepatitis B could have lipid disorders such as decreased plasma level of high-density lipoproteins (HDL). Furthermore, aberrations of lipid metabolism are often seen in the chronic hepatitis B infection. Plasma lipid profiles could be changed under HCC. In majority of the reports in HCC, plasma levels of triglycerides (TG), cholesterol, free fatty acids (FFA), HDL, low-density lipoproteins (LDL), lipoprotein (a) (Lp(a)), apolipoprotein AI (apoAI) and apoB were slight to significantly decreased, however, in some cases plasma levels of TG and Lp(a) might be increased. It has been suggested that analysis of plasma levels of lipids, lipoproteins and apolipoproteins in the patients suffered from HCC reflects on the hepatic cellular impairment status. Studies revealed that alterations seen in the plasma levels of lipids, lipoproteins and apolipoproteins reflecting patients' pathologic conditions. Decreased serum levels of cholesterol and apoAI may indicate a poor prognosis. Human leukaemic cells and certain tumor tissues have a higher receptor-mediated uptake of HDL and LDL than the corresponding normal cells or tissues. LDL and HDL have therefore been proposed as a carrier for the water-insoluble anti-cancer agents.
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| 6. |
- Jiang, J T, et al.
(författare)
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Treatment of advanced gastric cancer by chemotherapy combined with autologous cytokine-induced killer cells
- 2006
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Ingår i: Anticancer research. - 1791-7530. ; 26:3B, s. 2237-2242
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Tidskriftsartikel (refereegranskat)abstract
- The effects of autologous cytokine-induced killer (CIK) (CD3(+)CD56(+)) cells together with chemotherapy were investigated in patients who suffered from advanced gastric cancers (stage IV). Fifty-seven patients were divided into two groups: chemotherapy plus CIK biotherapy and chemotherapy alone. CIK cells were induced from autologous peripheral blood mononuclear cells in vitro and separated by flow cytometry and then transfused into the patients. The T-lymphocyte subgroups (CD3(+), CD4(+) or CD8(+)), CIK cells and NK cells (CD3(-)CD56(+)) were separated and determined by flow cytometry and the serum levels of MG7-Ag, CA72-4, CA19-9 and CEA were determined by ELISA or ECLIA. It was demonstrated that the cytotoxic activity of CIK cells reached a maximum between days 14 to 21 (68.7 +/- 10.9% and 65.3 +/- 10.4%, respectively). The amounts of CIK cells were gradually increased from day 0 to day 21 and slightly decreased in the further incubations. Thereafter, the CIK cells on days 14 to 21 (with the highest population of CIK cells) transfused back to the patients. The serum levels of the tumor markers were significantly decreased, the host immune function was increased and the short-term curative effect as well as the quality of life (QOL) were improved in the patients treated by chemotherapy plus CIK cells compared to the patients treated by chemotherapy alone. Moreover, the 2-year life-span was prolonged in the group treated by chemotherapy plus CIK cells compared to the group treated with chemotherapy alone. It is concluded that chemotherapy plus CIK cells has obvious benefits for patients who suffer from advanced gastric cancers.
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| 7. |
- Luo, Guanghua, et al.
(författare)
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Apolipoprotein M
- 2004
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Ingår i: Lipids in Health and Disease. - 1476-511X. ; 3
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Forskningsöversikt (refereegranskat)abstract
- Apolipoprotein M (apoM) is a 26-kDa protein that is mainly associated with high-density lipoprotein (HDL) in human plasma, with a small proportion present in triglyceride-rich lipoproteins (TGRLP) and low-density lipoproteins (LDL). Human apoM gene is located in p21.31 on chromosome 6 (chromosome 17, in mouse). Human apoM cDNA (734 base pairs) encodes 188-amino acid residue-long protein. It belongs to lipocalin protein superfamily. Human tissue expression array study indicates that apoM is only expressed in liver and in kidney and small amounts are found in fetal liver and kidney. In situ apoM mRNA hybridization demonstrates that apoM is exclusively expressed in the hepatocytes and in the tubule epithelial cells in kidney. Expression of apoM could be regulated by platelet activating factor (PAF), transforming growth factors (TGF), insulin-like growth factor (IGF) and leptin in vivo and/or in vitro. It has been demonstrated that apoM expression is dramatically decreased in apoA-I deficient mouse. Hepatocyte nuclear factor-1alpha (HNF-1alpha) is an activator of apoM gene promoter. Deficiency of HNF-1alpha mouse shows lack of apoM expression. Mutations in HNF-1alpha (MODY3) have reduced serum apoM levels. Expression of apoM is significantly decreased in leptin deficient (ob/ob) mouse or leptin receptor deficient (db/db) mouse. ApoM concentration in plasma is positively correlated to leptin level in obese subjects. These may suggest that apoM is related to the initiation and progression of MODY3 and/or obesity.
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| 8. |
- Luo, Guanghua, et al.
(författare)
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Expression and localization of apolipoprotein M in human colorectal tissues
- 2010
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Ingår i: Lipids in Health and Disease. - 1476-511X. ; 9
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Tidskriftsartikel (refereegranskat)abstract
- Background: It has been well documented that apolipoprotein M (apoM) is principally expressed in the liver and kidney. However we found that there was weak apoM expression in other tissues or organs too, which could not be ignored. In the present study, we therefore examined apoM expression in human colorectal tissues including cancer tissues, cancer adjacent normal tissues, polyp tissues and normal mucosa as well as inflammatory mucosa. Methods: Tissue samples were collected from patients who underwent surgical resection or endoscopic examination. ApoM mRNA levels were determined by the real-time RT-PCR and apoM protein mass were examined by the immunohistochemistry. Results: ApoM protein can be detected in all colorectal tissues. However, apoM protein mass were significantly lower in the cancer tissues than its matched adjacent normal tissues, polyp tissues, normal mucosa and inflammatory mucosa. In parallel, apoM mRNA levels in the colorectal cancer tissues (0.0536 +/- 0.0131) were also significantly lower than those in their adjacent normal tissues (0.1907 +/- 0.0563) (P = 0.033). Interestingly, apoM mRNA levels in colorectal cancer tissues were statistic significant higher in the patients with lymph node metastasis than the patients without lymph node metastasis (P = 0.008). Patients under Dukes' C and D stages had much higher apoM mRNA levels than patients under Dukes' A and B stages (P = 0.034). Conclusion: It is concluded that apoM could also be expressed in human colorectal tissues besides liver and kidney. ApoM mRNA levels in the colorectal cancer tissues were significantly increased in the patients with lymph node metastasis. Whether increased apoM expression in the patients with lymph node metastasis being related to patients' prognosis and the physiopathological importance of apoM expression in colorectal tissues need further investigation.
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| 9. |
- Luo, Guanghua, et al.
(författare)
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Genotyping of single nucleotide polymorphisms using base-quenched probe: A method does not invariably depend on the deoxyguanosine nucleotide
- 2009
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Ingår i: Analytical Biochemistry. - : Elsevier BV. - 1096-0309 .- 0003-2697. ; 386:2, s. 161-166
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Tidskriftsartikel (refereegranskat)abstract
- Most available methods for detecting single nucleotide polymorphisms (SNPs) are based principally on the system that can produce an increased fluorescence signal during hybridization. In the current study, we demonstrate a method of base-quenched probe for polymerase chain reaction (PCR) genotyping that requires only a pair of primers and one fluorescent probe and does not invariably depend on the deoxyguanosine nucleotide. This method further exploits the phenomenon of fluorescence quenching of fluorescent-labeled probe during hybridization to its complementary target gene's sequence. 6-Carboxyfluorescein (FAM) can be directly conjugated to a base of either adenine (A), thymine (T), cytosine (C), or guanine (G), referred to as A-, T-, C-, or G-quenched probe, respectively, at either the 5' or 3' end. For describing the method in detail, we chose apolipoprotein M (apoM) as a target gene in the current study. DNA sequencing analyses validated that all four types of base-quenched probes could provide unbiased genotyping results (K = 1, P = 0.000), although the maximum speed of fluorescence increase, max(dF/dT), when using the G-quenched probe method, was approximately twofold lower than the others (P < 0.0001). Moreover, we applied this method to detect another seven SNPs in the genomes of phospholipase A2, monocyte chemoattractant protein I (MCP1), and L-ficolin, further confirming our method. It is concluded that this method is precise, simple, and economic as well as suitable for large-scale genotyping Studies. (C) 2008 Elsevier Inc. All rights reserved.
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| 10. |
- Luo, Guanghua, et al.
(författare)
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Leptin inhibits apolipoprotein M transcription and secretion in human hepatoma cell line, HepG2 cells.
- 2005
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Ingår i: Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids. - : Elsevier BV. - 1388-1981. ; 1734:2, s. 198-202
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Tidskriftsartikel (refereegranskat)abstract
- Apolipoprotein M (apoM) is a novel apolipoprotein presented mostly in high-density lipoprotein (HDL) in human plasma. Previously we have reported that both leptin and leptin receptor are essential for apoM expression in vivo. The expression of apoM is lower in the leptin deficient (ob/ob) mouse and leptin receptor deficient (db/db) mouse than in the normal mouse. In the present study, however, we demonstrated that supra-physiological concentrations of recombinant leptin significantly inhibited apoM transcription and secretion in the human hepatoma cell line, HepG2 cells. Both Northern blotting and real-time RT-PCR were applied into the analyses of apoM mRNA levels, and compatible data were obtained. The inhibitory effect of leptin on apoM mRNA levels in HepG2 cells is dose dependent, i.e. 100 ng/mL of leptin decreased apoM mRNA levels by 30%, and 500 ng/mL of leptin decreased apoM mRNA levels about 50%. Even at a physiological concentration of leptin (10 ng/mL), apoM expression was decreased, and in parallel, the secretion of apoM into the medium was also decreased. Furthermore, we examined apoAI, apoB and apoE by Northern blotting analyses. The results demonstrated that leptin does not significantly influence the expressions of apoAI, apoB and apoE in HepC2 cells, suggesting that leptin has a specific regulatory effect on hepatic apoM transcription and secretion in vitro. The mechanism on the contradictory effects of leptin on apoM expression in vivo and in vitro needs further investigation.
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