دورية أكاديمية

Inhibition of miR-17~92 Cluster Ameliorates High Glucose-Induced Podocyte Damage

التفاصيل البيبلوغرافية
العنوان: Inhibition of miR-17~92 Cluster Ameliorates High Glucose-Induced Podocyte Damage
المؤلفون: Xiaobao Fan, Zhiming Hao, Zhenjiang Li, Xiaoming Wang, Jing Wang
المصدر: Mediators of Inflammation, Vol 2020 (2020)
بيانات النشر: Wiley, 2020.
سنة النشر: 2020
المجموعة: LCC:Pathology
مصطلحات موضوعية: Pathology, RB1-214
الوصف: The loss and damage of podocytes is an early feature of diabetic nephropathy (DN). The miR-17∼92 cluster was dysregulated in diabetic and polycystic kidney disease patients, but its role in DN is unclear. Hence, an in vitro study on the high glucose- (HG-) treated mouse podocytes (MPC5) was designed to elucidate the effect of miR-17∼92 cluster downregulation on cell viability, apoptosis, inflammation, fibrosis, and podocyte function. The results suggested that the miR-17∼92 cluster members miR-17-5p, miR-18a, miR-19a, miR-19b, miR-20a, and miR-92a were upregulated in the renal biopsy tissue of DN patients and HG-treated MPC5. The downregulation of the miR-17∼92 cluster effectively suppressed the cell apoptosis, inflammation, fibrosis, and podocyte dysfunction in HG-stimulated MPC5 cells. The bioinformatics analysis and rescue experiments showed that ABCA1 (ATP-binding cassette transporter A1) is an effector of the miR-17~92 cluster. Silence of ABCA1 inhibited the protective effect of the miR-17∼92 cluster downregulation on podocyte damage. In summary, this research indicated that the downregulation of the miR-17∼92 cluster ameliorates HG-induced podocyte damage via targeting ABCA1.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 0962-9351
1466-1861
Relation: https://doaj.org/toc/0962-9351; https://doaj.org/toc/1466-1861
DOI: 10.1155/2020/6126490
URL الوصول: https://doaj.org/article/264b152f6453482eb499b76564cdefe7
رقم الأكسشن: edsdoj.264b152f6453482eb499b76564cdefe7
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:09629351
14661861
DOI:10.1155/2020/6126490