Nestin((+)) cardiac myocyte-like cells were detected in the peri-infarct/infarct region of the ischemically damaged heart. The present study was undertaken to elucidate the phenotype and potential origin of nestin((+)) cardiac myocyte-like cells and identify stimuli implicated in their appearance.
In the infarcted human and rat heart, nestin((+)) cardiac myocyte-like cells were morphologically and structurally immature, exhibited a desmin-immunoreactive striated phenotype, expressed the beta1-adrenergic receptor and associated with an aberrant pattern of connexin-43 expression and/or organization.
Nestin((+)) cardiac myocyte-like cells were detected 24 hrs post ischemic injury and persisted in the infarcted rat heart for 9 months. In the normal rat heart, cardiac progenitor transcriptional factors Nkx2.5/GATA4 were detected in a subpopulation of nestin((+)) neural stem cells.
Following an ischemic insult, nestin((+))/Nkx2.5((+)) neural stem cells migrated to the peri-infarct/infarct region and appeared to be in a primordial state of differentiation to a nestin((+)) cardiac myocyte-like cell. The exposure of adult male rats to normobaric hypoxia (12% O2) for ten days failed to promote the appearance of nestin((+)) cardiac myocyte-like cells. Following osmotic pump delivery of isoproterenol to normal adult rats, nestin((+)) cardiac myocyte-like cells were detected, albeit the response was modest and secondary to tissue loss.
Thus, ischemia-induced appearance of nestin((+)) cardiac myocyte-like cells apparently represents an adaptive response to heal the infarcted heart. Nkx2.5/GATA4 expression in a subpopulation of resident neural stem cells provides the appropriate phenotype for their potential differentiation to a nestin((+)) cardiac myocyte-like cell.
"The phenotype and potential origin of nestin(+) cardiac myocyte-like cells following infarction".
J Appl Physiol. 2009 Aug 13; Beguin PC, El-Helou V, Assimakopoulos J, Clement R, Gosselin H, Brugada R, Villeneuve L, Rohlicek CV, Del Duca D, Lapointe N, Rouleau JL, Calderone A (Hubmed.org)
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In the infarcted human and rat heart, nestin((+)) cardiac myocyte-like cells were morphologically and structurally immature, exhibited a desmin-immunoreactive striated phenotype, expressed the beta1-adrenergic receptor and associated with an aberrant pattern of connexin-43 expression and/or organization.
Nestin((+)) cardiac myocyte-like cells were detected 24 hrs post ischemic injury and persisted in the infarcted rat heart for 9 months. In the normal rat heart, cardiac progenitor transcriptional factors Nkx2.5/GATA4 were detected in a subpopulation of nestin((+)) neural stem cells.
Following an ischemic insult, nestin((+))/Nkx2.5((+)) neural stem cells migrated to the peri-infarct/infarct region and appeared to be in a primordial state of differentiation to a nestin((+)) cardiac myocyte-like cell. The exposure of adult male rats to normobaric hypoxia (12% O2) for ten days failed to promote the appearance of nestin((+)) cardiac myocyte-like cells. Following osmotic pump delivery of isoproterenol to normal adult rats, nestin((+)) cardiac myocyte-like cells were detected, albeit the response was modest and secondary to tissue loss.
Thus, ischemia-induced appearance of nestin((+)) cardiac myocyte-like cells apparently represents an adaptive response to heal the infarcted heart. Nkx2.5/GATA4 expression in a subpopulation of resident neural stem cells provides the appropriate phenotype for their potential differentiation to a nestin((+)) cardiac myocyte-like cell.
"The phenotype and potential origin of nestin(+) cardiac myocyte-like cells following infarction".
J Appl Physiol. 2009 Aug 13; Beguin PC, El-Helou V, Assimakopoulos J, Clement R, Gosselin H, Brugada R, Villeneuve L, Rohlicek CV, Del Duca D, Lapointe N, Rouleau JL, Calderone A (Hubmed.org)
Related:
Cardiac Myocyte-Specific Expression of Inducible Nitric Oxide
The cannabinoid receptor type 2 promotes cardiac myocyte
Cardiac Myocyte-Specific Expression of Inducible Nitric Oxide
Reversal of cardiac myocyte dysfunction as a unique mechanism
Redox Sensing and Cardiac Myocyte Loss: Some Recent Insights
Left Ventricular Hypertrophy, Cardiac Myocyte Adaptation
NADPH oxidase signaling and cardiac myocyte function
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Increased Cardiac Myocyte Progenitors in Failing Human Hearts
