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Long non-coding RNA CDKN2B-AS1 regulates high glucose-induced human mesangial cell injury via regulating the

Jing Chang1, Yanming Yu2, Zhan Fang1

  • 1Department of Nephrology, Yantaishan Hospital, Yantai, Shandong, China.

Diabetology & Metabolic Syndrome
|December 10, 2020
PubMed
Abstract

Insights

Long non-coding RNA CDKN2B-AS1 promotes diabetic nephropathy by upregulating WNT2B via the miR-15b-5p pathway. This study reveals a novel mechanism in diabetic nephropathy development.

Area of Science:

  • Molecular Biology
  • Genetics
  • Nephrology

Background:

  • Diabetic nephropathy (DN) is a significant complication of diabetes.
  • Long non-coding RNA cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) is implicated in DN progression.
  • The precise regulatory mechanisms of CDKN2B-AS1 in DN remain largely unknown.

Purpose of the Study:

  • To elucidate the role and regulatory mechanisms of CDKN2B-AS1 in high glucose-induced human mesangial cell (HMC) dysfunction.
  • To investigate the interplay between CDKN2B-AS1, microRNA (miR)-15b-5p, and wingless-Type family member 2B (WNT2B) in the context of DN.

Main Methods:

  • Established a DN model using high glucose (HG)-induced HMCs.
  • Quantified expression levels of CDKN2B-AS1, miR-15b-5p, and WNT2B mRNA using qRT-PCR.
  • Assessed HMC viability, cell cycle, ECM accumulation, and inflammation via CCK-8, flow cytometry, western blotting, and ELISA.
  • Utilized dual-luciferase reporter assays to confirm interactions between CDKN2B-AS1, miR-15b-5p, and WNT2B.

Main Results:

  • CDKN2B-AS1 and WNT2B were upregulated, while miR-15b-5p was downregulated in DN patients' serum and HG-treated HMCs.
  • Inhibition of CDKN2B-AS1 ameliorated HG-induced HMC viability, cell cycle progression, ECM accumulation, and inflammation.
  • CDKN2B-AS1 directly targeted miR-15b-5p, influencing WNT2B expression.
  • MiR-15b-5p and WNT2B manipulations reversed the effects of CDKN2B-AS1 knockdown or overexpression, confirming the regulatory axis.

Conclusions:

  • CDKN2B-AS1 exacerbates HG-induced HMC dysfunction through the miR-15b-5p/WNT2B pathway.
  • This study provides a novel molecular mechanism underlying diabetic nephropathy development.
  • Targeting the CDKN2B-AS1/miR-15b-5p/WNT2B axis may offer therapeutic strategies for DN.
Keywords:
CDKN2B-AS1DNWNT2BmiR-15b-5p

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