RTN1 mediates progression of kidney disease by inducing ER stress

Ying Fan, Wenzhen Xiao, Zhengzhe Li, Xuezhu Li, Peter Y. Chuang, Belinda Jim, Weijia Zhang, Chengguo Wei, Niansong Wang, Weiping Jia, Huabao Xiong, Kyung Lee and John C. He ()
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Ying Fan: Icahn School of Medicine at Mount Sinai
Wenzhen Xiao: Icahn School of Medicine at Mount Sinai
Zhengzhe Li: Icahn School of Medicine at Mount Sinai
Xuezhu Li: Icahn School of Medicine at Mount Sinai
Peter Y. Chuang: Icahn School of Medicine at Mount Sinai
Belinda Jim: Jacobi Medical Center, Albert Einstein College of Medicine
Weijia Zhang: Icahn School of Medicine at Mount Sinai
Chengguo Wei: Icahn School of Medicine at Mount Sinai
Niansong Wang: Shanghai Jiao Tong University Affiliated Sixth People's Hospital
Weiping Jia: Shanghai Jiao Tong University Affiliated Sixth People's Hospital
Huabao Xiong: Immunology Institute, Icahn School of Medicine at Mount Sinai
Kyung Lee: Icahn School of Medicine at Mount Sinai
John C. He: Icahn School of Medicine at Mount Sinai

Nature Communications, 2015, vol. 6, issue 1, 1-17

Abstract: Abstract Identification of new biomarkers and drug targets for chronic kidney disease (CKD) is required for the development of more effective therapy. Here we report an association between expression of reticulon 1 (RTN1) and severity of CKD. An isoform-specific increase in the expression of RTN1A is detected in the diseased kidneys from mice and humans, and correlates inversely with renal function in patients with diabetic nephropathy. RTN1 overexpression in renal cells induces ER stress and apoptosis, whereas RTN1 knockdown attenuates tunicamycin-induced and hyperglycaemia-induced ER stress and apoptosis. RTN1A interacts with PERK through its N-terminal and C-terminal domains, and mutation of these domains prevents this effect on ER stress. Knockdown of Rtn1a expression in vivo attenuates ER stress and renal fibrosis in mice with unilateral ureteral obstruction, and also attenuates ER stress, proteinuria, glomerular hypertrophy and mesangial expansion in diabetic mice. Together, these data indicate that RTN1A contributes to progression of kidney disease by inducing ER stress.

Date: 2015
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DOI: 10.1038/ncomms8841

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