Oncotarget

Research Papers: Pathology:

Overexpressed cyclophilin B suppresses aldosterone-induced proximal tubular cell injury both in vitro and in vivo

Bin Wang, Lilu Lin, Haidong Wang, Honglei Guo, Yong Gu and Wei Ding _

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Oncotarget. 2016; 7:69309-69320. https://doi.org/10.18632/oncotarget.12503

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Abstract

Bin Wang1,*, Lilu Lin2,*, Haidong Wang3, Honglei Guo2, Yong Gu2 and Wei Ding2

1 Division of Nephrology, Huashan Hospital and Institute of Nephrology, Fudan University, Xuhui, Shanghai, P.R. China

2 Division of Nephrology, The Fifth People’s Hospital of Shanghai, Fudan University, Shanghai, P.R. China

3 College of Animal Science and Veterinary Medicine, Shanxi Agricultural University, Taigu, Shanxi, P.R. China

* These authors have contributed equally to this work

Correspondence to:

Wei Ding, email:

Keywords: tubular cell, oxidative stress, endoplasmic reticulum stress, apoptosis, aldosterone, Pathology Section

Received: June 30, 2016 Accepted: September 28, 2016 Published: October 06, 2016

Abstract

The renin-angiotensin-aldosterone system (RAAS) is overactivated in patients with chronic kidney disease. Oxidative stress and endoplasmic reticulum stress (ERS) are two major mechanisms responsible for aldosterone-induced kidney injury. Cyclophilin (CYP) B is a chaperone protein that accelerates the rate of protein folding through its peptidyl-prolyl cis-trans isomerase (PPIase) activity. We report that overexpression of wild-type CYPB attenuated aldosterone-induced oxidative stress (evidenced by reduced production of reactive oxygen species and improved mitochondrial dysfunction), ERS (indicated by reduced expression of the ERS markers glucose-regulated protein 78 [GRP78] and C/-EBP homologous protein [CHOP]), and tubular cell apoptosis in comparison with aldosterone-induced human kidney-2 (HK-2) cells. The in vivo study also yielded similar results. Hence, CYPB performs a crucial function in protecting cells against aldosterone-induced oxidative stress, ERS, and tubular cell injury via its PPIase activity.


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