Inflammation

, Volume 36, Issue 3, pp 738–749

Sca-1-Positive Cardiac Stem Cell migration in a Cardiac Infarction Model

Authors

  • Jingjin Liu
    • Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment
    • Depatment of CardiologySecond Affiliated Hospital of Harbin Medical University
  • Yongshun Wang
    • Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment
    • Depatment of CardiologySecond Affiliated Hospital of Harbin Medical University
  • Wenjuan Du
    • Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment
    • Depatment of CardiologySecond Affiliated Hospital of Harbin Medical University
    • Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment
    • Depatment of CardiologySecond Affiliated Hospital of Harbin Medical University
Article

DOI: 10.1007/s10753-013-9600-8

Cite this article as:
Liu, J., Wang, Y., Du, W. et al. Inflammation (2013) 36: 738. doi:10.1007/s10753-013-9600-8

Abstract

Adult myocardium has the capacity for repair and regeneration, which is derived from cardiac stem cells (CSCs). In this study, we assessed the migration and changes in numbers of Sca-1-positive CSCs after myocardial infarction (MI) in vivo and in vitro. In this study, we showed that in a rat MI model the CSCs emerged around the vessels near the peri-infarct zone and in the epicardium of the infarcted area. Four weeks after infarction, no differences in the expression of connexin 43 (Cx43) were observed in the peri-infarct and infarct zones. In vitro, we mimicked tissue ischemia and hypoxia by using a culture environment of 5 % O2 and a wound healing assay to monitor the migration of CSCs. In conclusion, under hypoxic conditions, the CSCs, conveyed by blood vessels, migrated from the niche to the infarct zone for repairing the damaged myocytes. The number of endogenous migrating CSCs was proportionate to the repair time after infarction, rather than the degree of infarction. Four weeks after MI, the expression of Cx43 was not altered in migratory CSCs, namely no enhanced gap-junctional communication with cardiomyocytes was seen in the CSCs. Further studies are necessary to delineate the molecular mechanisms that drive the migration of CSCs after MI.

KEY WORDS

cardiac stem cellsmyocardial infarctionmigrationregenerationhypoxia

Abbreviations

CSC

cardiac stem cell

MI

myocardial infarction

AMI

acute myocardial infarction

LAD

left anterior descending coronary artery

MACS

magnetic cell sorting

LV

left ventricle

LVEF

left ventricular ejection fraction

LVFS

left ventricular fractional shortening

Cx43

connexin 43

Copyright information

© Springer Science+Business Media New York 2013