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STIM2 knockdown protects against ischemia/reperfusion injury through reducing mitochondrial calcium overload and

Chen-Chen Tu1, Bao-Yan Wan1, Yong Zeng1

  • 1Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China.

Life Sciences
|June 15, 2019
PubMed

Insights

Stromal interactive molecule 2 (STIM2) upregulation exacerbates cardiomyocyte apoptosis after ischemia/reperfusion (I/R) injury. STIM2 knockdown protects heart cells by reducing calcium overload and preserving mitochondrial function.

Area of Science:

  • Cardiovascular Biology
  • Mitochondrial Medicine
  • Cellular Physiology

Background:

  • Mitochondrial dysfunction and calcium overload are key drivers of cardiomyocyte death during ischemia/reperfusion (I/R) injury.
  • Stromal interactive molecule 2 (STIM2), a calcium sensor regulating store-operated calcium entry (SOCE), has an unclear role in I/R injury.

Purpose of the Study:

  • To investigate the role of STIM2 in cardiomyocyte apoptosis following I/R injury.
  • To determine if STIM2 modulates mitochondrial calcium overload and function during I/R injury.

Main Methods:

  • Utilized H9c2 cells and primary neonatal cardiomyocytes as models for I/R injury.
  • Examined STIM2 and STIM1 expression levels post-I/R.
  • Assessed the effects of STIM2 knockdown on cell apoptosis, endoplasmic reticulum (ER) and mitochondrial calcium levels, and mitochondrial function.

Main Results:

  • STIM2, not STIM1, was upregulated in cardiomyocytes following I/R injury.
  • Knockdown of STIM2 significantly reduced H9c2 and primary cardiomyocyte apoptosis after I/R.
  • STIM2 knockdown alleviated mitochondrial calcium overload, decreased ER calcium release, and preserved mitochondrial function.

Conclusions:

  • STIM2 plays a critical role in mediating cardiomyocyte apoptosis and mitochondrial dysfunction during I/R injury.
  • Targeting STIM2 offers a potential therapeutic strategy for mitigating I/R injury by reducing mitochondrial calcium overload and preserving mitochondrial integrity.
Keywords:
Calcium overloadH9c2 cellIschemia/reperfusion injuryMitochondrial functionSTIM2

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