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Kv4.3 expression abrogates and reverses norepinephrine-induced myocyte hypertrophy by CaMKII inhibition

Yanggan Wang1, Thitima Keskanokwong2, Jun Cheng3

  • 1Department of Cardiology, Zhongnan Hospital of Wuhan University, Wuhan University, China; Medical Research Institute, Wuhan University, China; Department of Pediatrics, Emory University, Atlanta, GA 30322, USA.

Journal of Molecular and Cellular Cardiology
|November 22, 2018
PubMed

Insights

Kv4.3 protein reduction promotes cardiac hypertrophy by increasing CaMKII activity. Restoring Kv4.3 expression can prevent and reverse this hypertrophy, offering a potential therapeutic strategy for heart conditions.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Cell Biology

Background:

  • Down-regulation of Kv4.3 protein is a common characteristic of cardiac hypertrophy.
  • Kv4.3 reduction is proposed as a potential stimulator of cardiac hypertrophy.

Purpose of the Study:

  • To investigate if Kv4.3 expression can prevent or reverse norepinephrine (NE)-induced cardiac hypertrophy in neonatal rat ventricular myocytes (NRVMs).

Main Methods:

  • NRVMs were treated with NE to induce hypertrophy, monitoring changes in cell size, protein/DNA ratio, and specific molecular markers.
  • The effects of Kv4.3 expression and CaMKII inhibitors on NE-induced hypertrophy were assessed.
  • Key signaling pathways including CaMKII, calcineurin, PKA, and NFATc3 were analyzed.

Main Results:

  • NE treatment caused time-dependent myocyte hypertrophy, increased CaMKII and calcineurin activity, and reduced Kv4.3 expression.
  • CaMKII inhibitors partially blunted NE-induced hypertrophy and promoted regression.
  • Kv4.3 expression completely prevented NE-induced hypertrophy and led to regression, associated with reduced CaMKII activity and NFATc3 levels.

Conclusions:

  • Kv4.3 reduction mediates cardiac hypertrophy through excessive CaMKII activation.
  • Kv4.3 expression represents a potential therapeutic strategy for preventing and reversing cardiac hypertrophy induced by adrenergic stress.
Abstract

Keywords:
And myocytesCaMKIICalcineurinHypertrophyI(to) channelKv4.3

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