Bibliographic Details
| Title: |
Long non-coding RNA CDKN2B-AS1 regulates high glucose-induced human mesangial cell injury via regulating the miR-15b-5p/WNT2B axis |
| Authors: |
Jing Chang, Yanming Yu, Zhan Fang, Haiyan He, Dan Wang, Jian Teng, Lina Yang |
| Source: |
Diabetology & Metabolic Syndrome, Vol 12, Iss 1, Pp 1-11 (2020) |
| Publisher Information: |
BMC, 2020. |
| Publication Year: |
2020 |
| Collection: |
LCC:Nutritional diseases. Deficiency diseases |
| Subject Terms: |
DN, CDKN2B-AS1, miR-15b-5p, WNT2B, Nutritional diseases. Deficiency diseases, RC620-627 |
| More Details: |
Abstract Background Long non-coding RNA cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) has been reported to be related to diabetic nephropathy (DN) progression. However, the regulatory mechanisms of CDKN2B-AS1 in DN are unclear. Methods High glucose (HG) was used to induce human mesangial cells (HMCs) for establishing the DN model. Expression levels of CDKN2B-AS1, microRNA (miR)-15b-5p, wingless-Type family member 2B (WNT2B) mRNA in serum and HMCs were detected through quantitative real-time polymerase chain reaction (qRT-PCR). The viability and cell cycle progression of HMCs were determined with Cell Counting Kit-8 (CCK-8) or flow cytometry assays. The levels of several proteins and inflammatory factors in HMCs were analyzed by western blotting or enzyme-linked immunosorbent assay (ELISA). The relationship between CDKN2B-AS1 or WNT2B and miR-15b-5p was verified with dual-luciferase reporter assay. Results CDKN2B-AS1 and WNT2B were upregulated while miR-15b-5p was downregulated in serum of DN patients and HG-treated HMCs. CDKN2B-AS1 inhibition reduced HG-induced viability, cell cycle progression, ECM accumulation, and inflammation response in HMCs. CDKN2B-AS1 regulated WNT2B expression via competitively binding to miR-15b-5p. MiR-15b-5p inhibitor reversed CDKN2B-AS1 knockdown-mediated influence on viability, cell cycle progression, ECM accumulation, and inflammation response of HG-treated HMCs. The repressive effect of miR-15b-5p mimic on viability, cell cycle progression, ECM accumulation, and inflammation response of HG-treated HMCs was abolished by WNT2B overexpression. Conclusion CDKN2B-AS1 regulated HG-induced HMC viability, cell cycle progression, ECM accumulation, and inflammation response via regulating the miR-15b-5p/WNT2B axis, provided a new mechanism for understanding the development of DN. |
| Document Type: |
article |
| File Description: |
electronic resource |
| Language: |
English |
| ISSN: |
1758-5996 |
| Relation: |
https://doaj.org/toc/1758-5996 |
| DOI: |
10.1186/s13098-020-00618-z |
| Access URL: |
https://doaj.org/article/24afba7a5de44dbf978a767ce8ff1e5b |
| Accession Number: |
edsdoj.24afba7a5de44dbf978a767ce8ff1e5b |
| Database: |
Directory of Open Access Journals |
