Microglial neuropilin-1 promotes oligodendrocyte expansion during development and remyelination by trans-activating platelet-derived growth factor receptor.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
15 04 2021
Historique:
received: 16 01 2020
accepted: 08 03 2021
entrez: 16 4 2021
pubmed: 17 4 2021
medline: 4 5 2021
Statut: epublish

Résumé

Nerve-glia (NG2) glia or oligodendrocyte precursor cells (OPCs) are distributed throughout the gray and white matter and generate myelinating cells. OPCs in white matter proliferate more than those in gray matter in response to platelet-derived growth factor AA (PDGF AA), despite similar levels of its alpha receptor (PDGFRα) on their surface. Here we show that the type 1 integral membrane protein neuropilin-1 (Nrp1) is expressed not on OPCs but on amoeboid and activated microglia in white but not gray matter in an age- and activity-dependent manner. Microglia-specific deletion of Nrp1 compromised developmental OPC proliferation in white matter as well as OPC expansion and subsequent myelin repair after acute demyelination. Exogenous Nrp1 increased PDGF AA-induced OPC proliferation and PDGFRα phosphorylation on dissociated OPCs, most prominently in the presence of suboptimum concentrations of PDGF AA. These findings uncover a mechanism of regulating oligodendrocyte lineage cell density that involves trans-activation of PDGFRα on OPCs via Nrp1 expressed by adjacent microglia.

Identifiants

pubmed: 33859199
doi: 10.1038/s41467-021-22532-2
pii: 10.1038/s41467-021-22532-2
pmc: PMC8050320
doi:

Substances chimiques

Lysophosphatidylcholines 0
Platelet-Derived Growth Factor 0
platelet-derived growth factor A 0
Neuropilin-1 144713-63-3
Receptor, Platelet-Derived Growth Factor alpha EC 2.7.10.1

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2265

Subventions

Organisme : NINDS NIH HHS
ID : R01 NS073425
Pays : United States
Organisme : NIH HHS
ID : S10 OD016435
Pays : United States

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Auteurs

Amin Sherafat (A)

Department of Physiology and Neurobiology, University of Connecticut, Storrs, CT, USA.

Friederike Pfeiffer (F)

Department of Physiology and Neurobiology, University of Connecticut, Storrs, CT, USA.
Department of Physiology, University of Tübingen, Tübingen, Germany.

Alexander M Reiss (AM)

Department of Physiology and Neurobiology, University of Connecticut, Storrs, CT, USA.

William M Wood (WM)

Department of Physiology and Neurobiology, University of Connecticut, Storrs, CT, USA.

Akiko Nishiyama (A)

Department of Physiology and Neurobiology, University of Connecticut, Storrs, CT, USA. akiko.nishiyama@uconn.edu.
Institute for Systems Genomics, University of Connecticut, Storrs, CT, USA. akiko.nishiyama@uconn.edu.
The Connecticut Institute for the Brain and Cognitive Sciences, University of Connecticut, Storrs, CT, USA. akiko.nishiyama@uconn.edu.

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