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This Article Full Text Full Text (PDF) Supplemental Data All Versions of this Article: 2007-0715v1 26/6/1646    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints/Permissions Google Scholar Articles by Dawn, B. Articles by Bolli, R. PubMed PubMed Citation Articles by Dawn, B. Articles by Bolli, R.

TISSUE-SPECIFIC STEM CELLS

Transplantation of Bone Marrow-Derived Very Small Embryonic-Like Stem Cells Attenuates Left Ventricular Dysfunction and Remodeling After Myocardial Infarction

^aInstitute of Molecular Cardiology and
^bStem Cell Biology Program, University of Louisville, Louisville, Kentucky, USA

Key Words. Myocardial infarction • Myocardial regeneration • Very small embryonic-like stem cell • Stem cell • Bone marrow • Left ventricular function

Correspondence: Buddhadeb Dawn, M.D., Institute of Molecular Cardiology, University of Louisville, Louisville, Kentucky 40292, USA. Telephone: 502-852-7959; Fax: 502-852-7147; e-mail: buddha{at}louisville.edu; Roberto Bolli, M.D., Institute of Molecular Cardiology, University of Louisville, Louisville, Kentucky 40292, USA. Telephone: 502-852-1837; Fax: 502-852-6474; e-mail: rbolli{at}louisville.edu

Received August 27, 2007; accepted for publication March 31, 2008.
First published online in STEM CELLS EXPRESS   April 17, 2008.

Adult bone marrow (BM) contains Sca-1+/Lin–/CD45– very small embryonic-like stem cells (VSELs) that express markers of several lineages, including cardiac markers, and differentiate into cardiomyocytes in vitro. We examined whether BM-derived VSELs promote myocardial repair after a reperfused myocardial infarction (MI). Mice underwent a 30-minute coronary occlusion followed by reperfusion and received intramyocardial injection of vehicle (n= 11), 1 x 10⁵ Sca-1+/Lin–/CD45+ enhanced green fluorescent protein (EGFP)-labeled hematopoietic stem cells (n= 13 [cell control group]), or 1 x 10⁴ Sca-1+/Lin–/CD45– EGFP-labeled cells (n= 14 [VSEL-treated group]) at 48 hours after MI. At 35 days after MI, VSEL-treated mice exhibited improved global and regional left ventricular (LV) systolic function (echocardiography) and attenuated myocyte hypertrophy in surviving tissue (histology and echocardiography) compared with vehicle-treated controls. In contrast, transplantation of Sca-1+/Lin–/CD45+ cells failed to confer any functional or structural benefits. Scattered EGFP+ myocytes and capillaries were present in the infarct region in VSEL-treated mice, but their numbers were very small. These results indicate that transplantation of a relatively small number of CD45– VSELs is sufficient to improve LV function and alleviate myocyte hypertrophy after MI, supporting the potential therapeutic utility of these cells for cardiac repair.

Disclosure of potential conflicts of interest is found at the end of this article.