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Isolation and Kv Channel Recordings in Murine Atrial and Ventricular Cardiomyocytes
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Published on: March 12, 2013

Bone morphogenetic protein-4 contributes to the down-regulation of Kv4.3 K+ channels in pathological cardiac

Bo Sun1, Yue Sheng, Rong Huo

  • 1Department of Pharmacology, The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education, Harbin Medical University, Harbin 150086, PR China.

Biochemical and Biophysical Research Communications
|June 11, 2013
PubMed

Insights

Bone morphogenetic protein 4 (BMP4) reduces Kv4.3 K(+) channels in cardiac hypertrophy. This mechanism involves reactive oxygen species (ROS) and may offer therapeutic targets for heart disease.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Biochemistry

Background:

  • Kv4.3 K(+) channels are crucial for cardiac action potential repolarization.
  • Pathological cardiac hypertrophy is associated with decreased Kv4.3 K(+) channel expression.
  • Bone morphogenetic protein 4 (BMP4) expression is elevated in cardiac hypertrophy.

Purpose of the Study:

  • To investigate the role of BMP4 in the downregulation of Kv4.3 K(+) channels during cardiac hypertrophy.
  • To elucidate the underlying molecular mechanisms linking BMP4 to Kv4.3 K(+) channel reduction.

Main Methods:

  • In vitro studies using cultured cardiomyocytes treated with BMP4, BMP4 inhibitors (noggin, DMH1), NADPH oxidase inhibitor (apocynin), and radical scavenger (tempol).
  • In vivo studies involving transverse aortic constriction (TAC)-induced cardiac hypertrophy in mice with DMH1 infusion.
  • Assessment of Kv4.3 K(+) channel protein expression via Western blotting.

Main Results:

  • BMP4 treatment significantly reduced Kv4.3 K(+) channel protein expression in cardiomyocytes.
  • BMP4-induced downregulation of Kv4.3 K(+) channels was reversed by BMP4 inhibitors and by inhibiting NADPH oxidase/ROS production.
  • In vivo administration of DMH1 prevented the downregulation of Kv4.3 K(+) channels in TAC-induced cardiac hypertrophy.

Conclusions:

  • BMP4 contributes to the downregulation of Kv4.3 K(+) channels in pathological cardiac hypertrophy.
  • The mechanism likely involves the increased production of reactive oxygen species (ROS).
  • Targeting the BMP4-ROS pathway may represent a novel therapeutic strategy for cardiac hypertrophy.

Keywords:
Bone morphogenetic protein-4HypertrophyKv4.3 K(+) channel

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