Editorials |
From the Skirball Laboratory for Cardiovascular Cellular Therapeutics, Center for Cardiovascular Cell Therapy, Departments of Cardiovascular Medicine and Stem Cell Biology and Regenerative Medicine, Cleveland Clinic, Ohio.
Correspondence to Marc S. Penn, MD, PhD, Director, Skirball Laboratory for Cardiovascular Cellular Therapeutics and Center for Cardiovascular Cell Therapy, Department of Cardiovascular Medicine, J2, 9500 Euclid Ave, Cleveland, OH 44195. E-mail pennm@ccf.org
See related articles, pages 1209–1216
Key Words: stem cells myocardial infarction myocyte biology
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Since the original descriptions of the role of stromal cell-derived factor (SDF)-1 in recruiting bone marrow derived stem cells to the sites of vascular1 and myocardial injury,2 there has been increasing evidence of the broader importance of the SDF-1:CXCR4 axis in regulating myocardial repair following ischemic injury.2–6 In this issue of Circulation Research, Tang et al investigate the role of the SDF-1:CXCR4 axis in the recruitment of exogenously derived cardiac stem cells.7 They further investigate how cardiac stem cell exposure to hypoxia before their intravenous administration alters cardiac stem cell engraftment and subsequent effects on myocardial repair.
Cardiac stem cells were derived from cardiosphere cultures and were defined by as CLK (cardiosphere-derived c-Kit+ Lin–) cells. The cells were shown to have evidence of cardiac potential through the expression of green fluorescent protein under control of the Nkx2.5 promoter. The cells were administered intravenously 1 hour following permanent left anterior descending coronary artery ligation in the murine model of myocardial infarction.
In vitro studies demonstrated that CLK cells grown under normoxic conditions did not migrate significantly in response to SDF-1, nor was there significant engraftment of functional effects of these cells following the intravenous administration 1 hour after acute myocardial infarction. Conversely, culturing the CLK cells for 6 hours before harvest and infusion led to robust migration of the CLK cells in response to SDF-1 in vitro. Furthermore, the hypoxia treatment led to significant migration and engraftment of CLK cells following intravenous infusion and significant functional effects including decreased
Related Article:
Circ. Res. 2009 104: 1209-1216.
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