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Attenuation of ischemic myocardial injury and dysfunction by cardiac fibroblast-derived factor(s)

Kazuhiko Nakazato1, Wakako Naganuma, Kazuei Ogawa

  • 1Department of Cardiology and Hematology, Fukushima Medical University, Fukushima, Japan. nakazato@fmu.ac.jp

Fukushima Journal of Medical Science
|April 14, 2011
PubMed

Insights

Cardiac fibroblasts release substances that protect the heart from ischemia. This study identified an unknown cardioprotective factor in rat cardiac fibroblast-conditioned medium (CM) that mimics ischemic preconditioning.

Area of Science:

  • Cardiovascular Biology
  • Cellular Cardiology
  • Regenerative Medicine

Background:

  • Cardiac fibroblasts are abundant non-cardiomyocytes in the heart.
  • Fibroblasts secrete various signaling molecules impacting cardiac function.
  • The cardioprotective potential of fibroblast-derived substances against ischemic injury is largely unexplored.

Purpose of the Study:

  • To investigate the cardioprotective effects of cardiac fibroblast-conditioned medium (CM) on ischemic myocardium.
  • To elucidate the mechanisms underlying CM-mediated cardioprotection.
  • To identify the molecular weight and potential identity of the cardioprotective factor.

Main Methods:

  • In vitro assessment of cardiomyocyte viability under hypoxia with CM treatment.
  • Ex vivo evaluation of left ventricular (LV) function during global ischemia-reperfusion using Langendorff's preparation in rats.
  • Pharmacological inhibition of protein kinase C and mitochondrial ATP-sensitive K+ channels.
  • Fractionation of CM based on molecular weight and testing for cardioprotective activity.
  • Neutralization assay using an antibody against hepatocyte growth factor (HGF).

Main Results:

  • CM significantly increased cardiomyocyte viability under hypoxic conditions (41.4% vs. 20.5% in control).
  • CM treatment improved LV function post-ischemia-reperfusion, evidenced by reduced end-diastolic pressure and enhanced developed pressure.
  • Cardioprotection was attributed to a factor with molecular weight > 50,000 Da.
  • Inhibition of protein kinase C or mitochondrial K+ channels attenuated the protective effects.
  • Hepatocyte growth factor (HGF) was not identified as the primary cardioprotective agent.

Conclusions:

  • Cardiac fibroblast-conditioned medium (CM) possesses significant cardioprotective properties against ischemic injury.
  • The protective factor in CM appears to be a protein with a molecular weight greater than 50,000 Da.
  • The mechanism involves pathways modulated by protein kinase C and mitochondrial ATP-sensitive K+ channels.
  • An unknown cardioprotective substance, distinct from HGF, may be responsible for mimicking ischemic preconditioning.

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