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Long Noncoding RNA OIP5-AS1 Overexpression Promotes Viability and Inhibits High Glucose-Induced Oxidative Stress of

Haiyun Sun1, Chong Wang2, Ying Zhou2

  • 1Department of Endocrinology and Metabolism, The First Affiliated Hospital of Soochow University, Suzhou City, Jiangsu Province, 215006,China.

Endocrine, Metabolic & Immune Disorders Drug Targets
|December 31, 2020
PubMed
Abstract

Insights

Long noncoding RNA OIP5-AS1 (OIP5-AS1) enhances cardiomyocyte viability and reduces oxidative stress in diabetic cardiomyopathy (DCM). This occurs by regulating the microRNA-34a (miR-34a)/SIRT1 pathway, offering a potential therapeutic target for DCM.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Genetics

Background:

  • Diabetic cardiomyopathy (DCM) is a significant complication of diabetes, characterized by impaired cardiomyocyte function.
  • The role of long noncoding RNAs (lncRNAs) in the pathogenesis of DCM is an emerging area of research.

Purpose of the Study:

  • To investigate the effect of lncRNA OIP5-AS1 on cardiomyocyte viability and oxidative stress in the context of DCM.
  • To elucidate the molecular mechanism involving OIP5-AS1, microRNA-34a (miR-34a), and SIRT1 in DCM.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) to assess OIP5-AS1 and miR-34a expression.
  • In vitro simulation of DCM using high glucose (HG) treatment in H9c2 cells, followed by MTT assay for viability and assessment of reactive oxygen species (ROS), superoxide dismutase (SOD), and malondialdehyde (MDA) levels.
  • Dual-luciferase reporter assay and Western blot to confirm interactions and protein expression within the OIP5-AS1/miR-34a/SIRT1 axis.

Main Results:

  • OIP5-AS1 expression was decreased, while miR-34a expression was increased in DCM models.
  • OIP5-AS1 overexpression improved cardiomyocyte viability and attenuated oxidative stress markers (reduced ROS and MDA, increased SOD) in HG-treated cells.
  • miR-34a was confirmed to target both OIP5-AS1 and SIRT1, with miR-34a overexpression inhibiting SIRT1 protein levels. Feedback experiments showed miR-34a or SIRT1 inhibition counteracted the protective effects of OIP5-AS1.

Conclusions:

  • OIP5-AS1 overexpression enhances cardiomyocyte viability and reduces oxidative stress in DCM by modulating the miR-34a/SIRT1 pathway.
  • OIP5-AS1 represents a promising therapeutic target for the treatment of diabetic cardiomyopathy.
Keywords:
Diabetic cardiomyopathyOIP5-AS1SIRT1long noncoding RNAmicroRNA-34aoxidative stress.

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