Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2019 Sep 19;12:225. doi: 10.3389/fnmol.2019.00225

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2019 Baaklini, Rawji, Duncan, Ho and Plemel.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Importance of astrocyte regulation of remyelination. Following demyelination, astrocytes help regulate OPC behavior via the expression of extracellular matrix (ECM) molecules such as CSPGs, hyluronan, fibronectin, and tenacin C, endothelin-1 and growth factor secretion such as FGF2, brain-derived neurotrophic factor (BDNF), and PDGF. Endothelin-1, through autocrine and paracrine signaling, stimulates the expression of the notch ligand jagged1 that antagonizes remyelination. Astrocytes control the fate choice of OPCs following demyelination by antagonizing their differentiation into Schwann cells (SCs). Astrocytes may phagocytose myelin debris, but this has only been validated in vitro. They also express TNF-α, which binds to TNFR2 to promote remyelination.