



@article {3305,
	title = {Human umbilical cord tissue-derived mesenchymal stromal cells attenuate remodeling after myocardial infarction by proangiogenic, antiapoptotic, and endogenous cell-activation mechanisms},
	journal = {Stem Cell Research and Therapy},
	volume = {5},
	year = {2014},
	note = {Cited By (since 1996):2Export Date: 21 November 2014},
	month = {2014},
	abstract = {Introduction. Among the plethora of cells under investigation to restore a functional myocardium, mesenchymal stromal cells (MSCs) have been granted considerable interest. However, whereas the beneficial effects of bone marrow MSCs (BM-MSCs) in the context of the diseased heart are widely reported, data are still scarce on MSCs from the umbilical cord matrix (UCM-MSCs). Herein we report on the effect of UCM-MSC transplantation to the infarcted murine heart, seconded by the dissection of the molecular mechanisms at play. Methods. Human umbilical cord tissue-derived MSCs (UCX{\textregistered}), obtained by using a proprietary technology developed by ECBio, were delivered via intramyocardial injection to C57BL/6 females subjected to permanent ligation of the left descending coronary artery. Moreover, medium produced by cultured UCX{\textregistered} preconditioned under normoxia (CM) or hypoxia (CMH) was collected for subsequent in vitro assays. Results: Evaluation of the effects upon intramyocardial transplantation shows that UCX{\textregistered} preserved cardiac function and attenuated cardiac remodeling subsequent to myocardial infarction (MI). UCX{\textregistered} further led to increased capillary density and decreased apoptosis in the injured tissue. In vitro, UCX{\textregistered}-conditioned medium displayed (a) proangiogenic activity by promoting the formation of capillary-like structures by human umbilical vein endothelial cells (HUVECs), and (b) antiapoptotic activity in HL-1 cardiomyocytes subjected to hypoxia. Moreover, in adult murine cardiac Sca- 1{\textsection}ssup{\textsection}+{\textsection}esup{\textsection} progenitor cells (CPCs), conditioned medium enhanced mitogenic activity while activating a gene program characteristic of cardiomyogenic differentiation. Conclusions: UCX{\textregistered} preserve cardiac function after intramyocardial transplantation in a MI murine model. The cardioprotective effects of UCX{\textregistered} were attributed to paracrine mechanisms that appear to enhance angiogenesis, limit the extent of the apoptosis, augment proliferation, and activate a pool of resident CPCs. Overall, these results suggest that UCX{\textregistered} should be considered an alternative cell source when designing new therapeutic approaches to treat MI. {\textcopyright} 2014 Nascimento et al.; licensee BioMed Central Ltd.},
	url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84896713037\&partnerID=40\&md5=22fdca81d834ec78c8196552c3d250ae},
	author = {Nascimento, D.S. and Mosqueira, D. and Sousa, L.M. and Teixeira, M. and Filipe, M. and Resende, TP and Ara{\'u}jo, A.F. and Valente, M. and Almeida, J. and Martins, J.P. and Santos, J.M. and B{\'a}rcia, R.N. and Cruz, P. and Cruz, H. and Pinto-Do-{\'O}, P.}
}
