دورية أكاديمية

Early Growth Response 1 (Egr1) Is a Transcriptional Activator of NOX4 in Oxidative Stress of Diabetic Kidney Disease

التفاصيل البيبلوغرافية
العنوان: Early Growth Response 1 (Egr1) Is a Transcriptional Activator of NOX4 in Oxidative Stress of Diabetic Kidney Disease
المؤلفون: Fang Hu, Meng Xue, Yang Li, Yi-Jie Jia, Zong-Ji Zheng, Yan-Lin Yang, Mei-Ping Guan, Liao Sun, Yao-Ming Xue
المصدر: Journal of Diabetes Research, Vol 2018 (2018)
بيانات النشر: Wiley, 2018.
سنة النشر: 2018
المجموعة: LCC:Diseases of the endocrine glands. Clinical endocrinology
مصطلحات موضوعية: Diseases of the endocrine glands. Clinical endocrinology, RC648-665
الوصف: Background. NADPH oxidase 4 (NOX4) plays a major role in renal oxidative stress of diabetic kidney disease (DKD). NOX4 was significantly increased in Egr1-expressing fibroblasts, but the relationship between Egr1 and NOX4 in DKD is unclear. Methods. For the evaluation of the potential relationship between Egr1 and NOX4, both were detected in HFD/STZ-induced mice and HK-2 cells treated with TGF-β1. Then, changes in NOX4 expression were detected in HK-2 cells and mice with overexpression and knockdown of Egr1. The direct relationship between Egr1 and NOX4 was explored via chromatin immunoprecipitation (ChIP). Results. We found increased levels of Egr1, NOX4, and α-SMA in the kidney cortices of diabetic mice and in TGF-β1-treated HK-2 cells. Overexpression or silencing of Egr1 in HK-2 cells could upregulate or downregulate NOX4 and α-SMA. ChIP assays revealed that TGF-β1 induced Egr1 to bind to the NOX4 promoter. Finally, Egr1 overexpression or knockdown in diabetic mice could upregulate or downregulate the expression of NOX4 and ROS, and α-SMA was also changed. Conclusion. Our study provides strong evidence that Egr1 is a transcriptional activator of NOX4 in oxidative stress of DKD. Egr1 contributes to DKD by enhancing EMT, in part by targeting NOX4.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2314-6745
2314-6753
24074977
Relation: https://doaj.org/toc/2314-6745; https://doaj.org/toc/2314-6753
DOI: 10.1155/2018/3405695
URL الوصول: https://doaj.org/article/ca37d13d46a2407497753fce70508fb2
رقم الأكسشن: edsdoj.37d13d46a2407497753fce70508fb2
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:23146745
23146753
24074977
DOI:10.1155/2018/3405695