MicroRNA-125b alleviates hydrogen-peroxide-induced abnormal mitochondrial dynamics in HT22 cells by inhibiting p53

Yan Huang1,2, Songyun Deng1, Yuhang Ai1,2

  • 1Department of Critical Care Medicine, Xiangya Hospital, Central South University, Changsha, People's Republic of China, 410008.

Metabolic Brain Disease
|January 21, 2021
PubMed

Insights

Micro-RNA125b (miR-125b) protects against oxidative stress by suppressing tumor protein p53 (p53) expression, thereby alleviating mitochondrial damage in HT22 cells. This reveals a novel mechanism for miR-125b in regulating mitochondrial homeostasis.

Area of Science:

  • Molecular Biology
  • Neuroscience
  • Cell Biology

Background:

  • Mitochondrial dynamics are crucial for cellular health.
  • Oxidative stress can lead to mitochondrial dysfunction and cell death.
  • The interplay between micro-RNA125b (miR-125b) and tumor protein p53 (p53) in oxidative stress is not fully understood.

Purpose of the Study:

  • To investigate the role and mechanism of miR-125b and p53 in oxidative stress-induced mitochondrial damage.
  • To elucidate the interaction between miR-125b and p53 in HT22 cells under oxidative stress.

Main Methods:

  • Immortalized mouse hippocampal HT22 cells were treated with hydrogen peroxide (H2O2) to induce oxidative stress.
  • miR-125b and p53 expression levels were analyzed.
  • Mitochondrial damage and cell death were assessed.
  • Overexpression of miR-125b and p53 was performed to evaluate their effects.
  • Confocal and electron microscopy were utilized.

Main Results:

  • H2O2 treatment led to decreased miR-125b, increased p53, mitochondrial damage, and cell death.
  • Overexpression of miR-125b reduced mitochondrial damage and p53 levels.
  • Overexpression of p53 negated the protective effects of miR-125b on mitochondria.

Conclusions:

  • miR-125b alleviates oxidative stress-induced mitochondrial dysfunction in HT22 cells by suppressing p53.
  • This study presents a new model for miR-125b's influence on mitochondrial dynamics and homeostasis.