Academic Journal

Rtn1a-Mediated Endoplasmic Reticulum Stress in Podocyte Injury and Diabetic Nephropathy

التفاصيل البيبلوغرافية
العنوان: Rtn1a-Mediated Endoplasmic Reticulum Stress in Podocyte Injury and Diabetic Nephropathy
المؤلفون: Fan, Ying, Zhang, Jing, Xiao, Wenzhen, Lee, Kyung, Li, Zhengzhe, Wen, Jiejun, He, Li, Gui, Dingkun, Xue, Rui, Jian, Guihua, Sheng, Xiaohua, He, John Cijiang, Wang, Niansong
المصدر: Scientific Reports ; volume 7, issue 1 ; ISSN 2045-2322
بيانات النشر: Springer Science and Business Media LLC
سنة النشر: 2017
الوصف: We previously reported a critical role of reticulon (RTN) 1A in mediating endoplasmic reticulum (ER) stress in kidney tubular cells and the expression of RTN1A correlates with the renal function and the severity of kidney injury in patients with diabetic nephropathy (DN). Here, we determined the roles of RTN1A and ER stress in podocyte injury and DN. We used db/db mice with early unilateral nephrectomy (Unx) as a murine model of progressive DN and treated mice with tauroursodeoxycholic acid (TUDCA), a specific inhibitor of ER stress. We found increased expression of RTN1A and ER stress markers in the kidney of db/db-Unx mice. Treatment of TUDCA not only attenuated proteinuria and kidney histological changes, but also ameliorated podocyte and glomeruli injury in diabetic mice, which were associated with reduction of RTN1A and ER stress marker expression in the podocytes of TUDCA-treated mice. In vitro , we showed RTN1A mediates albumin-induced ER stress and apoptosis in human podocytes. A positive feedback loop between RTN1A and CHOP was found leading to an enhanced ER stress in podocytes. Our data suggest that ER stress plays a major role in podocyte injury in DN and RTN1A might be a key regulator of ER stress in podocytes.
نوع الوثيقة: article in journal/newspaper
اللغة: English
DOI: 10.1038/s41598-017-00305-6
الاتاحة: http://dx.doi.org/10.1038/s41598-017-00305-6
https://www.nature.com/articles/s41598-017-00305-6.pdf
https://www.nature.com/articles/s41598-017-00305-6
Rights: https://creativecommons.org/licenses/by/4.0 ; https://creativecommons.org/licenses/by/4.0
رقم الانضمام: edsbas.58402FFB
قاعدة البيانات: BASE
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