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A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
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MORN4 protects cardiomyocytes against ischemic injury via MFN2-mediated mitochondrial dynamics and mitophagy

Jinrun Zhou1, Honghong Liu1, Tianliang Zhang2

  • 1Shandong Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Sciences, Shandong University, Qingdao, 266237, PR China.

Free Radical Biology & Medicine
|January 22, 2023
PubMed

Insights

MORN4 protein protects the heart from injury by regulating mitochondrial dynamics and mitophagy. Sphingosylphosphorylcholine (SPC) enhances this protective effect, offering new therapeutic targets for myocardial infarction.

Area of Science:

  • Cardiovascular Biology
  • Mitochondrial Biology
  • Cellular Dynamics

Background:

  • Mitochondrial fission-fusion imbalance contributes to ischemic heart injury and cardiomyocyte apoptosis by affecting mitophagy.
  • Mitochondrial dynamics regulation is a key therapeutic strategy for ischemic heart diseases.
  • MORN motifs play roles in heart diseases and chloroplast fission.

Purpose of the Study:

  • Investigate the role of MORN repeat-containing protein 4 (MORN4) in myocardial infarction (MI), ischemic cardiomyocyte apoptosis, mitochondrial dynamics, and mitophagy.
  • Elucidate the mechanism by which MORN4 influences heart injury and the therapeutic effect of Sphingosylphosphorylcholine (SPC).

Main Methods:

  • Utilized a myocardial infarction (MI) mouse model.
  • Performed MORN4 knockdown experiments.
  • Investigated the interaction between MORN4, MFN2, and ROCK2.
  • Assessed cardiac function, injury, fibrosis, apoptosis, and mitophagy.

Main Results:

  • MORN4 knockdown exacerbated cardiac injury, fibrosis, and dysfunction in MI mice.
  • Sphingosylphosphorylcholine (SPC) alleviated ischemic cardiomyocyte apoptosis and heart injury by increasing MORN4 levels.
  • MORN4 directly binds to MFN2 and promotes MFN2 S442 phosphorylation via ROCK2, mediating beneficial mitophagy.
  • SPC enhanced MORN4-MFN2 binding and mitophagy.

Conclusions:

  • MORN4 plays a protective role in ischemic heart injury.
  • SPC activates the MORN4-MFN2 axis to regulate myocardial mitochondrial homeostasis during ischemia.
  • The MORN4-MFN2 pathway presents novel therapeutic targets for improving myocardial ischemia tolerance and treating acute myocardial infarction.
Keywords:
MFN2MORN4Mitochondrial dynamicsMitophagyMyocardial infarctionSphingosylphosphorylcholine

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