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

Chabot, Andréanne; Méus, Marc-André; Hertig, Vanessa; Duquette, Natacha; Calderone, Angelino

doi:10.1186/1475-2840-12-114

Cited by 4 publications

(2 citation statements)

References 34 publications

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“…Ischemic injury to the beating transplanted rat heart led to the de novo synthesis of neurofilament-M (+) -fibers physically associated with nestin (+) -processes emanating from neural progenitor/stem cells (Béguin et al, 2011 ). The neurogenic response of cardiac resident neural progenitor/stem cells post-MI is characterized by the initial expression of GAP43 (+) -fibers physically associated with nestin (+) -processes and subsequently replaced by neurofilament-M (+) -fibers (Chabot et al, 2013 ). The temporal neurogenic response is consistent with previous studies revealing that GAP43 expression represents an early event of neurogenesis during learning and following regeneration of injured peripheral nerves (Leu et al, 2010 ; Grasselli et al, 2011 ).…”

Section: Neural Progenitor/stem Cells and The Neurogenic Response Durmentioning

confidence: 99%

The Biological Role of Nestin(+)-Cells in Physiological and Pathological Cardiovascular Remodeling

Calderone

2018

Front. Cell Dev. Biol.

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The intermediate filament protein nestin was identified in diverse populations of cells implicated in cardiovascular remodeling. Cardiac resident neural progenitor/stem cells constitutively express nestin and following an ischemic insult migrate to the infarct region and participate in angiogenesis and neurogenesis. A modest number of normal adult ventricular fibroblasts express nestin and the intermediate filament protein is upregulated during the progression of reparative and reactive fibrosis. Nestin depletion attenuates cell cycle re-entry suggesting that increased expression of the intermediate filament protein in ventricular fibroblasts may represent an activated phenotype accelerating the biological impact during fibrosis. Nestin immunoreactivity is absent in normal adult rodent ventricular cardiomyocytes. Following ischemic damage, the intermediate filament protein is induced in a modest population of pre-existing adult ventricular cardiomyocytes bordering the peri-infarct/infarct region and nestin(+)-ventricular cardiomyocytes were identified in the infarcted human heart. The appearance of nestin(+)-ventricular cardiomyocytes post-myocardial infarction (MI) recapitulates an embryonic phenotype and depletion of the intermediate filament protein inhibits cell cycle re-entry. Recruitment of the serine/threonine kinase p38 MAPK secondary to an overt inflammatory response after an ischemic insult may represent a seminal event limiting the appearance of nestin(+)-ventricular cardiomyocytes and concomitantly suppressing cell cycle re-entry. Endothelial and vascular smooth muscle cells (VSMCs) express nestin and upregulation of the intermediate filament protein may directly contribute to vascular remodeling. This review will highlight the biological role of nestin(+)-cells during physiological and pathological remodeling of the heart and vasculature and discuss the phenotypic advantage attributed to the intermediate filament protein.

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Section: Neural Progenitor/stem Cells and The Neurogenic Response Durmentioning

confidence: 99%

The Biological Role of Nestin(+)-Cells in Physiological and Pathological Cardiovascular Remodeling

Calderone

2018

Front. Cell Dev. Biol.

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“…The associations between Nes and Gap43 had been shown to exist in the regeneration of cardiac nestin (+) cells [63] and in acute spinal cord injury [64] . We assume that the regulated coexpression changes of Nes, Ngfr and Gap43 are important as early-acting factors in regenerating SGNs.…”

Section: Nestin-associated Genesmentioning

confidence: 99%

Expression of nestin-associated genes in the inner ear of newborn rats following injury and hypoxia

Gross

Mazurek

2015

Inflamm Cell Signal

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We used organotypic cultures of the stria vascularis (SV), the organ of Corti (OC) and the modiolus (MOD) of newborn rats to analyze the differential expression levels and responses of cytoskeletal, myelin-and neural growth factor-associated genes following preparatory injury and hypoxia. The transcript mRNA levels of the neurofilaments Nefl, Nefm, the microtubule-associated proteins Mapt, Map1a, Map2, and of the myelin basic protein Mbp decrease during 24 h in a coordinated way across the MOD and OC regions. The increased cell death rate in the MOD region is associated with an increased expression of Nes, the transcript encoding the intermediate filament nestin, and of the neural growth factor receptor Ngfr, the growth-associated protein 43 Gap43 and the Purkinje cell protein Pcp4. The correlation analysis revealed close associations between Nes expression and genes involved in apoptotic and necrotic cell death (caspase Casp3, calpains Capn1, Capn2, Capns1), the glutamate pathway (glutamate receptor NMDA associated protein 1 Grina, glial high affinity glutamate transporter Slc1a3), cytoskeletal genes (Nefm, Map2, Map1a, Mbp), transcription factors (hypoxia inducible factor Hif-1a, jun proto-oncogene Jun, brain expressed myelocytomatosis B-myc, HES family bHLH transcription factor 1 Hes-1, forkhead-box D3 Foxd3) and neural growth factors (Ngfr, Gap43 and Pcp4). The unique response and the composition of the Nes cluster made us conclude that the expression of cell-death-associated genes and the regeneration-associated genes takes place in a coordinated way, and differs between the MOD and the OC/SV regions.

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Nestin downregulation in rat vascular smooth muscle cells represents an early marker of vascular disease in experimental type I diabetes

Tardif

Hertig

Dumais

et al. 2014

Cardiovasc Diabetol

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BackgroundNestin was reported to directly contribute to cell proliferation and the intermediate filament protein was detected in vascular smooth muscle cells. In experimental type I diabetes, nestin downregulation in the heart was identified as an incipient pathophysiological event. The following study tested the hypothesis that dysregulation of nestin expression in vascular smooth muscle cells represented an early event of vascular disease in experimental type I diabetes.Methods/ResultsIn the carotid artery and aorta of adult male Sprague-Dawley rats, a subpopulation of vascular smooth muscle cells co-expressed nestin and was actively involved in the cell cycle as reflected by the co-staining of nuclear phosphohistone-3. The infection of aortic vascular smooth muscle cells with a lentivirus containing a shRNAmir directed against nestin significantly reduced protein expression and concomitantly attenuated basal DNA synthesis. Two weeks following injection of adult male Sprague-Dawley rats with streptozotocin, the endothelial response of aortic rings to acetylcholine, vascular morphology and the total density of vascular smooth muscle cells in the vasculature of type I diabetic rats were similar to normal rats. By contrast, nestin protein levels and the density of nestin(+)/phosphohistone-3(+)-vascular smooth muscle cells were significantly reduced in type I diabetic rats. The in vivo observations were recapitulated in vitro as exposure of vascular smooth muscle cells to 30 mM D-glucose inhibited DNA synthesis and concomitantly reduced nestin protein expression.ConclusionsHyperglycaemia-mediated nestin downregulation and the concomitant reduction of cycling vascular smooth muscle cells represent early markers of vascular disease in experimental type I diabetes.Electronic supplementary materialThe online version of this article (doi:10.1186/s12933-014-0119-6) contains supplementary material, which is available to authorized users.

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

Cited by 4 publications

References 34 publications

The Biological Role of Nestin(+)-Cells in Physiological and Pathological Cardiovascular Remodeling

The Biological Role of Nestin(+)-Cells in Physiological and Pathological Cardiovascular Remodeling

Expression of nestin-associated genes in the inner ear of newborn rats following injury and hypoxia

Nestin downregulation in rat vascular smooth muscle cells represents an early marker of vascular disease in experimental type I diabetes

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