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The elevated serum S100A8/A9 during acute myocardial infarction is not of cardiac myocyte origin

Chang-Qing Du1, Lin Yang, Jie Han

  • 1Institute of Cardiology, the First Affiliated Hospital, School of Medicine, Zhejiang University, 79 Qing Chun Road, Hangzhou, Zhejiang 310003, People's Republic of China.

Inflammation
|September 3, 2011
PubMed

Insights

Increased S100A8/A9 proteins after acute myocardial infarction (AMI) do not originate from cardiac myocytes. Studies show ischemia and hypoxia activate NF-kappaB but do not alter S100A8/A9 expression in heart cells.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Inflammation Research

Background:

  • Elevated circulating S100A8/A9 levels are observed in patients post-acute myocardial infarction (AMI).
  • The cellular origin of these proteins, specifically cardiac myocytes, following ischemic events remains undetermined.

Purpose of the Study:

  • To investigate whether ischemia induces S100A8 and S100A9 expression in cardiac myocytes.
  • To determine if cardiac myocytes contribute to the circulating S100A8/A9 pool after myocardial infarction.

Main Methods:

  • Western blot analysis and quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR).
  • Experiments utilized isolated rat hearts (spontaneously hypertensive and Wistar-Kyoto) subjected to global ischemia.
  • Neonatal rat cardiac myocytes were exposed to hypoxic conditions.

Main Results:

  • Myocardial S100A8 and S100A9 protein and mRNA levels did not increase following ischemia in either rat model.
  • S100A8/A9 protein levels remained unchanged in hypoxic neonatal cardiac myocytes.
  • NF-kappaB activation was observed in response to ischemia and hypoxia in a time-dependent manner.

Conclusions:

  • Cardiac myocytes are not the source of elevated serum S100A8/A9 concentrations observed after AMI.
  • While ischemia/hypoxia activate NF-kappaB in cardiac cells, they do not stimulate S100A8/A9 production within these cells.

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