Abstract
All-trans retinoic acid (ATRA) is a critical component in cell processes such as cell growth, differentiation and apoptosis, and it is also crucial in the regulation of extracellular matrix (ECM) deposition. Prohibitin (PHB) can regulate cell proliferation, apoptosis and differentiation. The current study investigated whether ATRA regulated PHB is induced by hypoxia/reoxygenation injury in renal tubular epithelial cells (RTEC), using gene interference treatments (knockdown or overexpression of RARα). Our results indicate that ATRA can augment the expression of RARα and PHB proteins and reduce the expression of TGF-β1, FN and Col-IV proteins. PHB expression was reduced in an ATRA treated RARα- group, and TGF-β1, FN and Col-IV were up-regulated compared to the ATRA treated RARα+ group. We postulate that ATRA can induce the PHB expression by RARα in hypoxia/reperfusion related RTEC injury.
Highlights
Renal interstitial fibrosis (RIF) is a common condition involved in the progression of end-stage renal failure which is characterized by the excessive deposition of extracellular matrix (ECM) [1, 2]
Correlation analysis Correlation analysis indicated that RARα protein level was positively correlated with PHB, superoxide dismutase (SOD), and GSH (r= 0.728, 0.816, 0.822; each P
RARα protein level was positively correlated with PHB, GSH, and SOD, but positively correlated with TGF-β1, FN, ColIV, ROS, and MDA
Summary
Materials and MethodsRenal interstitial fibrosis (RIF) is a common condition involved in the progression of end-stage renal failure which is characterized by the excessive deposition of extracellular matrix (ECM) [1, 2]. The current study investigated whether ATRA regulated PHB is induced by hypoxia/reoxygenation injury in renal tubular epithelial cells (RTEC), using gene interference treatments (knockdown or overexpression of RARα). PHB expression was reduced in an ATRA treated RARα- group, and TGF-β1, FN and Col-IV were up-regulated compared to the ATRA treated RARα+ group.
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