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- Title
Adiponectin attenuates Ang II-induced TGFβ1 production in human mesangial cells via an AMPK-dependent pathway.
- Authors
Tan, Min; Tang, Gongyao; Rui, Hongliang
- Abstract
Glomerulosclerosis is a key element in end-stage renal failure. Angiotensin II (Ang II) plays an important role in modulating cell growth and extracellular matrix (ECM) synthesis and degradation. Adiponectin, a protein derived from adipocytes, is primarily involved in regulating glucose levels and fatty acid break down. It has recently been shown to have antiatherosclerotic and anti-inflammatory properties. However, the role of adiponectin as a renoprotective agent has not been fully explored. We herein examine the effect of adiponectin on Ang II-induced TGFβ1 and ECM production in human renal mesangial cells (HRMCs) and explore the signaling pathway involved. In this study, we found that both adiponectin receptor 1 and adiponectin receptor 2 are expressed in HRMCs. Adiponectin (10 µg/mL) attenuated the stimulatory effect of Ang II on TGF-β1 and fibronectin. Furthermore, adiponectin activated the AMP-activated protein kinase (AMPK), and the AMPK-specific inhibitor (compound C) blocked AMPK activation. We also determined that compound C blocked the inhibitory effect of adiponectin on Ang II-stimulated TGFβ1 and fibronectin production. In summary, these results demonstrate that adiponectin suppresses Ang II-induced synthesis of ECM in mesangial cells via activation of the AMPK pathway. Based on our data, we suggest that this mechanism could delay the progression of kidney disease.
- Subjects
ADIPONECTIN; GLOMERULOSCLEROSIS; KIDNEY failure; CELL growth; EXTRACELLULAR matrix; FAT cells; ANTI-inflammatory agents
- Publication
Biotechnology & Applied Biochemistry, 2015, Vol 62, Issue 6, p848
- ISSN
0885-4513
- Publication type
Article
- DOI
10.1002/bab.1323