Forced myocardin expression primes cardiac and smooth muscle transcription patterning in human mesenchymal stem cells

Abstract

See article by van Tuyn et al. [7] (pages 245–255) in this issue. Loss of cardiomyocytes during myocardial infarction or hereditary cardiomyopathies may represent a major determinant in the progression toward heart failure. The reported ability of haematopoietic bone marrow cells to afford myocardial regeneration after direct injection in experimental animals [1] has triggered a number of clinical trials in humans. Nevertheless, the initial observations and the scientific underpinning of the human trials have been challenged by a number of studies using a foreign gene, LacZ or GFP, to track the fate of haematopoietic stem cells after transplant into normal and/or injured mouse hearts [2,3]. In these studies, no transdifferentiation into cardiomyocytes was detectable, and stem-cell-engrafted hearts showed no overt increase in cardiomyocytes compared to sham-engrafted hearts. These results indicate that haematopoietic stem cells do not readily acquire a cardiac phenotype, raising a cautionary note for clinical studies of infarct repair. These controversial results emphasize the need to assess whether cardiac lineage-committable cells may be comprised within the bone marrow, and prompt further studies to dissect the signals … *Present address: S. Orsola-Malpighi Hospital, Institute of Cardiology, Via Massarenti N.g, 40138 Bologna, Italy. Tel.: +39 051 6363605; fax: +39 051 344859. Email address: cvent{at}libero.it