Adiponectin antagonizes angiotensin Ⅱ -induced extracelluar matrix production of human renal mesangial cells
10.3760/cma.j.issn.1001-7097.2011.08.009
- VernacularTitle:脂联素拮抗血管紧张素Ⅱ诱导系膜细胞细胞外基质产生
- Author:
Min TAN
;
Yipu CHEN
;
Gongyao TANG
;
Hongliang RUI
- Publication Type:Journal Article
- Keywords:
Adiponectin;
Angiotensin Ⅱ;
Transforming growth factor betal;
Mesangial cells;
Fibronectin
- From:
Chinese Journal of Nephrology
2011;27(8):591-596
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of adiponectin on angiotensin Ⅱ-induced extracellular matrix production of mesangial cells(MCs) and its possible signaling pathway.Methods RT-PCR and indirect immunofluorescence examination were performed to detect the adiponectin receptors in MCs.Quantitative real-time PCR and enzyme-linked immunosorbent assay (ELISA) were used to observe the effects of adiponectin on angiotensin Ⅱ-induced transforming growth factor β1(TGF-β1) and fibronectin production of MCs.Western blotting was used to measure the ratio of p-AMPK to total AMPK.Results(1)Adiponectin receptors 1 and 2 were found in MCs. (2)The up-regulated mRNA and protein expression of TGF-β1 and fibronectin in MCs induced with 10-7 mol/L angiotensin Ⅱ (Ang Ⅱ) was significantly inhibited by 10 mg/L adiponectin (P＜0.05).(3)The p-AMPK/AMPK ratio was significantly increased after incubation with adiponectin for 15 min and 30 min(vs 0 min, P＜0.05), which suggested that adiponectin could activate the AMPK signaling pathway in MCs.The activation of AMPK signaling pathway was blocked by 40 μmol/L compound C, a specific inhibitor of AMPK. (4)The inhibitory effects of adiponectinonangiotensin Ⅱ-upregulatedTGF-β1andfibronectinexpressioninMCswere significantly relieved by 40 μmol/L compound C (P＜0.05).Conclusions There are adiponectin receptors 1 and 2 in MCs.Adiponectin has inhibitory effects on the angiotensin Ⅱ-upregulated TGF-β1and fibronectin expression in MCs.AMPK signaling pathway may play an important role in the effects of adiponectin above-mentioned.
