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Ries, C.* ; Stark, T.* ; Boulat, B.* ; Ruhwedel, T.* ; Delling, J.P.* ; Infante, A.M.* ; von Poblotzki, J.T.* ; Ulivi, A.F.* ; von Mücke-Heim, I.A.* ; Chang, S.C.-E. ; Sakimura, K.* ; Itoi, K.* ; Nestvogel, D.B.* ; Attardo, A.* ; Czisch, M.* ; Nave, K.A.* ; Möbius, W.* ; Dimou, L.* ; Deussing, J.M.*

Neuropeptide CRH prevents premature differentiation of OPCs following CNS injury and in early postnatal development.

Cell Rep. 44:116474 (2025)
Publ. Version/Full Text Research data DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
The role of neuropeptides and their receptors in oligodendrocyte (OL) progenitor cells (OPCs) has been largely overlooked so far. Here, we describe a new subpopulation of corticotropin-releasing hormone (CRH)-expressing OPCs. Brain injury rapidly induces transient CRH expression in OPCs that aggregate around injury sites and exhibit an elevated capacity to differentiate into myelinating OLs. As target cells, we identified CRH receptor type 1 (CRHR1)-expressing OPCs, which show a decreased differentiation velocity. CRH/CRHR1 system inactivation increases the speed of OL generation but compromises their long-term survival after acute injury. Under non-injury conditions, CRH/CRHR1 system deficiency leads to increased early postnatal oligodendrogenesis and alterations in adult myelination. Altogether, we show that OPC-derived CRH not only actively influences the injury environment through interaction with CRHR1-expressing OPCs but also identify the G-protein coupled receptor CRHR1 as a critical modulator of oligodendrogenesis during early postnatal development with lasting effects on adult myelination.
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Publication type Article: Journal article
Document type Scientific Article
Keywords Cp: Neuroscience ; Crh ; Crhr1 ; Opcs ; Brain Injury ; Corticotropin-releasing Hormone ; Myelination ; Neuropeptides ; Oligodendrocytes ; Reporter Mouse Models ; Stress; Impaired Stress-response; Progenitor-cell; Neurons; Brain; Oligodendrocytes; Mice; Transmission; Myelination; Hormone; Death
ISSN (print) / ISBN 2211-1247
e-ISSN 2211-1247
Journal Cell Reports
Quellenangaben Volume: 44, Issue: 11, Pages: , Article Number: 116474 Supplement: ,
Publisher Cell Press
Publishing Place 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
Reviewing status Peer reviewed
Institute(s) Helmholtz Pioneer Campus (HPC)
Grants Gunter Sachs Donation
International Max Planck Research School for Translational Psychiatry
Max Planck Society