Nestin expression is upregulated in the fibrotic rat heart and is localized in collagen-expressing mesenchymal cells and interstitial CD31(+)- cells.

Renal and lung fibrosis was characterized by the accumulation of collagen-immunoreactive mesenchymal cells expressing the intermediate filament protein nestin. The present study tested the hypothesis that nestin expression was increased in the hypertrophied/fibrotic left ventricle of suprarenal abdominal aorta constricted adult male Sprague-Dawley rats and induced in ventricular fibroblasts by pro-fibrotic peptide growth factors. Nestin protein levels were upregulated in the pressure-overloaded left ventricle and expression positively correlated with the rise of mean arterial pressure.

Nestin Expressed by Pre-Existing Cardiomyocytes Recapitulated in Part an Embryonic Phenotype; Suppressive Role of p38 MAPK.

Nestin -cardiomyocytes were identified in the ischemically damaged human/rodent heart, albeit the cellular source, and signaling events implicated in the appearance of the intermediate filament protein remained undefined. Expression of the enhanced green fluorescent protein (EGFP) driven by the second intron of the nestin gene identified a subpopulation of EGFP/nestin cells that differentiated to a vascular phenotype in the peri-infarct/infarct region of post-MI mice albeit the transgene was not detected in nestin -cardiomyocytes. α-MHC-driven expression of the reporter mCherry was detected in troponin-T - and nestin -cardiomyocytes in the peri-infarct/infarct region of post-MI mice.

Nestin is a marker of lung remodeling secondary to myocardial infarction and type I diabetes in the rat.

Upregulation of the intermediate filament protein nestin was identified in a subpopulation of fibroblasts during reactive and reparative fibrosis and directly contributed to the enhanced proliferative phenotype. The present study tested the hypothesis that nestin was expressed in lung fibroblasts and the pattern of expression represented a distinct marker of pulmonary remodeling secondary to myocardial infarction and type I diabetes. Nestin((+)) fibroblasts were detected in rat lungs and a subpopulation exhibited a myofibroblast phenotype delineated by the co-expression of smooth muscle α-actin.

The neurogenic response of cardiac resident nestin(+) cells was associated with GAP43 upregulation and abrogated in a setting of type I diabetes.

Background: Cardiac nestin(+) cells exhibit properties of a neural progenitor/stem cell population characterized by the de novo synthesis of neurofilament-M in response to ischemic injury and 6-hydroxydopamine administration. The induction of growth associated protein 43 (GAP43) was identified as an early event of neurogenesis. The present study tested the hypothesis that the de novo synthesis of neurofilament-M by nestin(+) cells was preceded by the transient upregulation of GAP43 during the acute phase of reparative fibrosis in the infarcted male rat heart.