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Deshpande, S.S.* ; Malik, S.C.* ; Conforti, P.* ; Lin, J.d.* ; Chu, Y.H.* ; Nath, S.* ; Greulich, F. ; Dumbach, M.A.* ; Uhlenhaut, N.H. ; Schachtrup, C.*

P75 neurotrophin receptor controls subventricular zone neural stem cell migration after stroke.

Cell Tissue Res., DOI: 10.1007/s00441-021-03539-z (2021)
Verlagsversion DOI PMC
Open Access Gold (Paid Option)
Creative Commons Lizenzvertrag
Stroke is the leading cause of adult disability. Endogenous neural stem/progenitor cells (NSPCs) originating from the subventricular zone (SVZ) contribute to the brain repair process. However, molecular mechanisms underlying CNS disease-induced SVZ NSPC-redirected migration to the lesion area are poorly understood. Here, we show that genetic depletion of the p75 neurotrophin receptor (p75NTR−/−) in mice reduced SVZ NSPC migration towards the lesion area after cortical injury and that p75NTR−/− NSPCs failed to migrate upon BDNF stimulation in vitro. Cortical injury rapidly increased p75NTR abundance in SVZ NSPCs via bone morphogenetic protein (BMP) receptor signaling. SVZ-derived p75NTR−/− NSPCs revealed an altered cytoskeletal network- and small GTPase family-related gene and protein expression. In accordance, BMP-treated non-migrating p75NTR−/− NSPCs revealed an altered morphology and α-tubulin expression compared to BMP-treated migrating wild-type NSPCs. We propose that BMP-induced p75NTR abundance in NSPCs is a regulator of SVZ NSPC migration to the lesion area via regulation of the cytoskeleton following cortical injury.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Korrespondenzautor
Schlagwörter Bone Morphogenetic Protein ; Cytoskeleton ; Ischemic Stroke ; Neurotrophin Receptor ; Stem Cell Migration ; Vascular Damage; Adult Brain; Tgf-beta; Astrocytes; P75(ntr); Differentiation; Neurogenesis; Expression; Neurons; Niche; Precursors
ISSN (print) / ISBN 0044-3794
e-ISSN 1432-0878
Verlag Springer
Verlagsort One New York Plaza, Suite 4600, New York, Ny, United States
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Förderungen German Research Foundation
Deutscher Akademischer Austauschdienst fellowship