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MicroRNA-328 is involved in the effect of selenium on hydrogen peroxide-induced injury in H9c2 cells

Xiaolin Zheng1, Xiaoyan Hu1, Tangdong Ge1

  • 1Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, Heilongjiang, 150081, People's Republic of China.

Journal of Biochemical and Molecular Toxicology
|May 26, 2017
PubMed

Insights

Selenium protects cardiac cells from oxidative stress-induced apoptosis by modulating microRNA-328 (miR-328). This study shows selenium enhances cell viability and antioxidant enzyme activity, while miR-328 plays a key role in the protective mechanism.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • Oxidative Stress Research

Background:

  • Oxidative stress is a key factor in cardiac cell apoptosis.
  • Antioxidants and microRNAs (miRNAs) are implicated in cellular protection and death pathways.
  • Understanding miRNA involvement in selenium's protective effects against oxidative stress is crucial.

Purpose of the Study:

  • To investigate the role of miRNAs in selenium's protective effects against oxidative stress-induced apoptosis in cardiac cells.
  • To elucidate the specific mechanism involving miR-328 in sodium selenite's action.
  • To analyze the impact of sodium selenite on oxidative stress markers and apoptosis.

Main Methods:

  • Cell viability assays, superoxide dismutase (SOD) activity, and malondialdehyde (MDA) concentration measurements.
  • Flow cytometry for apoptosis evaluation and Fura-2AM for intracellular calcium (Ca2+) concentration.
  • Analysis of miR-328 levels and its downstream effects on ATP2A2 and Ca2+.

Main Results:

  • Sodium selenite ameliorated hydrogen peroxide (H2O2)-induced apoptosis and improved antioxidant enzyme expression (glutathione peroxidase, thioredoxin reductase).
  • Selenium pretreatment enhanced SOD activity and reduced MDA levels.
  • Both H2O2 and sodium selenite treatments altered miR-328 levels; miR-328 overexpression promoted apoptosis, reduced ATP2A2, and increased Ca2+.

Conclusions:

  • Selenium, via sodium selenite, protects cardiac cells against H2O2-induced oxidative stress and apoptosis.
  • MicroRNA-328 is identified as a key mediator in selenium's cardioprotective effects.
  • Modulation of miR-328 influences apoptosis, ATP2A2 expression, and intracellular Ca2+ levels in H9c2 cells.
Keywords:
apoptosismicroRNA-328oxidative stressselenium

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