期刊
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
卷 302, 期 1, 页码 H1-H9出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00716.2011
关键词
ischemia; stem cells; myofibroblasts; cardiac regeneration
资金
- Heart and Stroke Foundation of Canada and Quebec
- Canadian Diabetes Association
Calderone A. Nestin(+) cells and healing the infarcted heart. Am J Physiol Heart Circ Physiol 302: H1-H9, 2012. First published October 14, 2011; doi:10.1152/ajpheart.00716.2011.-Scar formation following an ischemic insult to the heart is referred to as reparative fibrosis and represents an essential physiological response to heal the damaged myocardium. The biological events of reparative fibrosis include inflammation, the deposition of collagen by myofibroblasts, sympathetic innervation, and angiogenesis. Several studies have further reported that scar formation was associated with the recruitment of neural crest-derived cardiac resident nestin(+) cells that display characteristics consistent with a neural progenitor/stem cell phenotype. During the reparative fibrotic response, these nestin(+) cells participate in neural remodeling and represent a novel cellular substrate of angiogenesis. In addition, a subpopulation of nestin(+) cells identified in the normal heart expressed cardiac progenitor transcriptional factors and may directly contribute to myocardial regeneration following ischemic damage. Nestin protein was also detected in endothelial cells of newly formed blood vessels in the scar and may represent a marker of revascularization. Lastly, nestin was induced in a subpopulation of smooth muscle alpha-actin(+) scar-derived myofibroblasts, and the expression of the intermediate filament protein may provide a proliferative advantage. Collectively, these data demonstrate that diverse populations of nestin(+) cells participate in cardiac wound healing.
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