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Nuclear cardiac myosin light chain 2 modulates NADPH oxidase 2 expression in myocardium: a novel function beyond

Yi-Shuai Zhang1, Bin Liu, Xiu-Ju Luo

  • 1Department of Pharmacology, School of Pharmaceutical Sciences, Central South University, Changsha, 410078, China.

Basic Research in Cardiology
|May 19, 2015
PubMed

Insights

Nuclear cardiac myosin light chain 2 (MYL2) acts as a transcription factor, increasing NADPH oxidase 2 (NOX2) expression after heart ischemia-reperfusion (IR) injury. This phosphorylation-dependent mechanism enhances oxidative stress and myocardial damage.

Area of Science:

  • Cardiovascular Biology
  • Molecular Mechanisms of Disease
  • Oxidative Stress

Background:

  • NADPH oxidase 2 (NOX2) expression is upregulated in myocardium following ischemia-reperfusion (IR) injury.
  • The precise molecular mechanisms driving NOX2 upregulation post-IR remain largely unknown.
  • Cardiac myosin light chain 2 (MYL2) is a known myosin regulatory subunit.

Purpose of the Study:

  • To investigate if nuclear MYL2 functions as a transcription factor regulating NOX2 expression in a phosphorylation-dependent manner after myocardial IR.
  • To elucidate the molecular mechanisms by which nuclear MYL2 influences NOX2 transcription.

Main Methods:

  • Utilized a rat model of myocardial IR injury and H9c2 cell hypoxia-reoxygenation (HR) injury models.
  • Examined phosphorylation status of nuclear MYL2 (p-MYL2), NOX2 expression, and reactive oxygen species (ROS) levels.
  • Employed molecular biology techniques including co-immunoprecipitation (Co-IP), chromatin immunoprecipitation (ChIP), DNA pull-down, and luciferase reporter assays.
  • Investigated the effects of myosin light chain kinase (MLCK) inhibition and MYL2 knockdown.

Main Results:

  • Myocardial IR and HR injury models showed increased NOX2 expression, elevated H₂O₂ levels, and increased nuclear p-MYL2.
  • Inhibition of MLCK or MYL2 knockdown attenuated these increases.
  • Nuclear p-MYL2 was found to bind the NOX2 gene promoter region (AGCTCC sequence).
  • Nuclear p-MYL2 interacts with RNA polymerase II and transcription factor IIB to form a transcription preinitiation complex, activating NOX2 transcription.

Conclusions:

  • Nuclear MYL2 plays a critical role in myocardial IR injury by transcriptionally upregulating NOX2 expression.
  • Phosphorylation of MYL2 is essential for its function as a transcription factor promoting NOX2 expression.
  • This mechanism enhances oxidative stress, contributing to myocardial damage post-IR.

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