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Intracellular and Extracellular Effects of S100B in the Cardiovascular Response to Disease

James N Tsoporis1, Forough Mohammadzadeh, Thomas G Parker

  • 1Division of Cardiology, Department of Medicine, Keenan Research Centre, Li Ka Shing Knowledge Institute, St. Michael's Hospital, University of Toronto, Toronto, ON, Canada M5B 1W8.

Cardiovascular Psychiatry and Neurology
|July 31, 2010
PubMed

Insights

S100B protein influences heart attack recovery. While it can worsen cell death, reducing S100B may protect the heart and blood vessels.

Area of Science:

  • Biochemistry
  • Cardiology
  • Molecular Biology

Background:

  • S100B is a calcium-binding protein with intracellular and extracellular roles.
  • S100B expression increases in the heart after myocardial infarction.
  • Its dual functions present potential therapeutic targets for cardiovascular diseases.

Purpose of the Study:

  • To investigate the role of S100B in cardiac and vascular responses, particularly after myocardial infarction.
  • To explore the mechanisms underlying S100B's effects on cardiac hypertrophy, apoptosis, and vascular smooth muscle cell function.
  • To assess the therapeutic potential of targeting S100B in cardiovascular diseases.

Main Methods:

  • Studied S100B expression in human and rat myocardial infarction models.
  • Utilized neonatal rat myocyte cultures and transgenic mice for forced S100B expression.
  • Investigated S100B knockout effects on cardiac function and smooth muscle cell behavior.
  • Examined extracellular S100B mechanisms involving the receptor for advanced glycation end products (RAGE) and downstream signaling pathways (ERK1/2, p53).

Main Results:

  • Overexpressing S100B inhibited cardiac hypertrophy but increased myocyte apoptosis post-myocardial infarction.
  • Knocking out S100B augmented hypertrophy, reduced apoptosis, and preserved cardiac function.
  • S100B expression in aortic smooth muscle cells inhibited proliferation and response to adrenergic stimulation.
  • Extracellular S100B induced apoptosis via RAGE, activating ERK1/2 and p53 signaling.

Conclusions:

  • S100B plays a complex, context-dependent role in cardiovascular pathophysiology.
  • Modulating S100B activity offers a promising therapeutic strategy for myocardial infarction and vascular diseases.
  • Targeting both intracellular and extracellular functions of S100B could be beneficial for treating cardiac and vascular conditions.

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