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Published on: February 16, 2015

Syndecan-4 signalling inhibits apoptosis and controls NFAT activity during myocardial damage and remodelling

Frank Echtermeyer1, Thomas Harendza, Svenja Hubrich

  • 1Department of Anesthesiology and Intensive Care Medicine, Hannover Medical School, Carl-Neuberg Str. 1, 30625 Hannover, Germany.

Cardiovascular Research
|June 3, 2011
PubMed
Abstract

Insights

Syndecan-4 (Sdc4) deficiency worsens early heart attack damage but improves left ventricular (LV) function and geometry later. Intercepting the Sdc4 pathway benefits LV function post-myocardial infarction.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Proteoglycan Research

Background:

  • Myocardial infarction (MI) impairs left ventricular (LV) function via cardiomyocyte death and remodeling.
  • Syndecan-4 (Sdc4) expression increases post-MI, but its cardiac role is unclear.

Purpose of the Study:

  • To investigate the function of Sdc4 in the heart during myocardial ischemia and infarction.
  • To characterize the effects of Sdc4 deficiency on cardiac response to injury.

Main Methods:

  • Utilized Sdc4-deficient (Sdc4(-/-)) and wild-type mice subjected to myocardial ischemia-reperfusion and permanent infarction models.
  • Assessed cardiomyocyte apoptosis, extracellular signal-regulated kinase (ERK) activation, and nuclear factor of activated T cells (NFAT) pathway activation.
  • Evaluated LV geometry and function using echocardiography.

Main Results:

  • Sdc4 deficiency exacerbated myocardial damage and cardiomyocyte apoptosis post-ischemia-reperfusion, linked to reduced ERK activation.
  • NFAT pathway activation, cardiomyocyte hypertrophy, and rcan1.4 transcription increased in Sdc4(-/-) mice.
  • Despite initial damage, Sdc4(-/-) mice showed improved LV geometry and function 7 days post-MI.

Conclusions:

  • Sdc4 deficiency promotes infarct expansion and hypertrophic remodeling during early infarct healing.
  • Targeting the Sdc4 pathway demonstrates net beneficial effects on LV function after myocardial infarction and ischemia-reperfusion injury.

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