Journal of Cell Science & Therapy
Open Access
ISSN: 2157-7013
+44 1300 500008
ISSN: 2157-7013
+44 1300 500008
Abdel Rahim A. Hamad
Scientific Tracks Abstracts: J Cell Sci Ther
Scar formation in the ischemically damaged heart is denoted as reparative fi brosis and represents an essential physiological response to heal the damaged myocardium. During the reparative fi brotic response, a previously unidentifi ed population of nestin (+) cells was detected in the infarct region. Th ese nestin (+) cells represent a resident cardiac population, are neural crest-derived, and migrate to the ischemic region. Employing a nestin-GFP transgenic mouse in which the GFP cDNA was placed between the nestin promoter (5.8 kb of the fl anking region) and the nestin enhancer (1.8 kb) of the second intron, a GFP signal was detected in cardiac nestin (+) cells. Th ese cardiac resident nestin (+) cells grow as spheres in the presence of bFGF/EGF and diff erentiate to a neuronal phenotype when cultured in the appropriate induction medium. Th e injection of cardiac nestin (+) cells into the infarcted rat heart revealed that a subpopulation was capable of diff erentiating to a vascular cell leading to de novo blood vessel formation in the scar. Furthermore, a subpopulation of cardiac nestin (+) cells was capable of diff erentiating to a neuronal-like phenotype in the ischemically damaged rat heart, characterized by the synthesis of neurofi lament-M (+) fi bres. Lastly, nestin (+) cells were detected in the viable myocardium and scar of the infarcted human heart and morphologically resembled neural crest-derived cells identifi ed in the rodent heart. Th ese data demonstrate that the adult heart contains a resident population of nestin (+) cells that exhibit a neural stem cell phenotype and directly participate in the angiogenic and neurogenic responses of reparative fi brosis following an ischemic insult
Angelino Calderone completed his Ph.D in 1992 at the Universit� de Montr�al and continued his post-doctoral studies at the Brigham & Women?s Hospital under the tutelage of Dr. Wilson Colucci. Dr. Calderone is presently a Professor in the department of Physiology at the Universit� de Montr�al, af fi liated with the Montreal Heart Institute and Chercheur-Boursier National of the FRSQ (Fonds de recherche en sant� du Qu�bec). During his career, Dr. Calderone has published 71 papers in the cardiovascular fi eld examining ventricular function and remodelling in cardiac disease states