کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
11987963 | 1051594 | 2018 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
miR-423-5p suppresses high-glucose-induced podocyte injury by targeting Nox4
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Podocyte injury plays crucial roles in the pathogenesis of diabetic nephropathy (DN). Aberrant microRNAs (miRNAs) have been suggested to contribute to podocyte injury. However, whether miR-423-5p could alleviate high glucose (HG)-mediated podocyte injury and the underlying mechanisms remains unclear. In this study, we found that patients with DN have reduced miR-423-5p and elevated Nicotinamide adenine dinucleotide phosphate oxidase 4 (Nox4) expressions in clinical renal tissues, and HG induced Nox4 but suppressed miR-423-5p expressions in cultured podocytes in a time-dependent manner. Moreover, overexpression of miR-423-5p antagonized HG-stimulated podocyte injury by enhancing cell viability, inhibiting reactive oxygen species (ROS) production, suppressing cell apoptosis, reducing inflammatory activity, and repressing cytoskeleton damage accompanied with alternations of podocyte specific proteins. Furthermore, functional assays substantiated that Nox4 was a direct target and negatively regulated by miR-423-5p. Additionally, restoration of Nox4 impeded the protective effect of miR-423-5p on podocyte injury via activation of p38 MAPK pathway. Therefore, this study manifested that miR-423-5p overexpression protected HG-induced podocyte damage by inhibiting ROS generation via targeting Nox4, providing a potential therapeutic strategy against DN.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 505, Issue 2, 28 October 2018, Pages 339-345
Journal: Biochemical and Biophysical Research Communications - Volume 505, Issue 2, 28 October 2018, Pages 339-345
نویسندگان
Yuxiang Xu, Jiuzhi Zhang, Li Fan, Xiaowen He,