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Related Experiment Videos

c-kit dysfunction impairs myocardial healing after infarction.

Massimo Cimini1, Shafie Fazel, Sun Zhuo

  • 1Division of Cardiovascular Surgery, Toronto General Hospital, University Health Network, University of Toronto, Ontario, Canada.

Circulation
|September 14, 2007
PubMed
Summary
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Bone marrow c-kit receptor function is crucial for cardiac repair after myocardial infarction (MI). Enhancing c-kit+ cell infiltration may improve heart healing and reduce infarct expansion.

Area of Science:

  • Cardiovascular Biology
  • Hematology
  • Regenerative Medicine

Background:

  • The role of c-kit receptor function in bone marrow stem cells is investigated for its potential in cardiac repair.
  • Myocardial infarction (MI) triggers a complex healing process where bone marrow-derived cells may play a significant role.

Purpose of the Study:

  • To assess the importance of c-kit receptor function in bone marrow for cardiac remodeling and repair following myocardial infarction (MI).
  • To investigate the impact of c-kit+ cells on infarct expansion, vascularization, and myofibroblast response in the infarcted heart.

Main Methods:

  • Utilized Kit(W)/Kit(W-v) c-kit mutant mice and wild-type littermates to study cardiac remodeling post-coronary ligation.
  • Assessed ventricular dilation, infarct expansion, smooth muscle alpha-actin expressing cells, and CD31 expressing blood vessels using microscopy and flow cytometry.

Related Experiment Videos

  • Employed bone marrow transplantation from wild-type to mutant mice to evaluate the rescue effect of functional c-kit+ cells.

    • Main Results:

    • Mutant mice lacking functional c-kit exhibited significantly greater ventricular dilation and infarct expansion compared to wild-type controls.
    • A marked reduction in proliferating and total smooth muscle alpha-actin expressing cells and CD31 expressing blood vessels was observed in mutant mice.
    • Bone marrow transplantation restored vascularization and myofibroblast populations in mutant mice, leading to reduced infarct expansion.

    Conclusions:

    • Bone marrow c-kit function is critical for the myofibroblast repair response in infarcted hearts.
    • Interventions aimed at increasing c-kit+ cell infiltration show promise for potentiating endogenous repair, preventing infarct expansion, and improving cardiac function after MI.