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1 Department of Physiology and Biophysics, Dalhousie University, Halifax, Nova Scotia, Canada
2 Department of Surgery, Dalhousie University, Halifax, Nova Scotia, Canada
3 Department of Pediatrics, Dalhousie University, Halifax, Nova Scotia, Canada
4 Department of Physiology, University of Manitoba, Winnipeg, Manitoba, Canada
* To whom correspondence should be addressed. E-mail: Magda.Horackova{at}dal.ca.
The adult heart injured by an ischemic episode has a limited capacity to regenerate. We administered three types of adult guinea pig cells (cardiomyocytes, cardiac fibroblasts and skeletal myoblasts) to compare their suitability for repair of acute myocardial infarction. Using
confocal fluorescent microscopy and a variety of specific immunomarkers and echo cardiography, we have provided anatomical evidence for the viability of such cells and their possible functional beneficial effects. All cells were transfected with adenovirus containing 
galactosidase gene such that their migration from the site of injections could be traced. Both freshly isolated cardiomyocytes (CM), as well as cardiac fibroblasts (CF), were found concentrated in the infarcted zone; they survived for at least two weeks post-transplantation. Transplanted CM were regularly striated and grew long projections that could form gap-junctions with the native CM, as evidenced by labeling for connexin 43. In addition, their transplantation resulted in an increased angiogenesis in the infarcted areas. In contrast transplanted CF did not appear to make any gap-junctional contacts with native CM nor did they enhance local angiogenesis. Skeletal myoblasts (Mb) cultured for 7 days and transfected Mb, were identified 7 days post-transplantation in the infarcted area. During that time and thereafter they proliferated and differentiated into myotubes that formed new regularly striated myofibers which occupied
most (50-70%) of the infarcted area by the 2-3 weeks. These newly formed myofibres maintained their skeletal muscle origin, as evidenced by their capacity to express myogenin and fast skeletal myosin. Such skeletal phenotype appeared to downregulate with time, Mb partially transdifferentiated into a cardiac phenotype as indicated by labeling for cardiac-specific troponin T and cardiac MHC. By the 3 week post-transplantation, new myofibres formed apparent rd contacts with the native CM via "putative gap-junction" expressing connexin 43. The myocardial performance of the animals successfully transplantated with myoblasts was improved.
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