Mechanical stretch induces myelin protein loss in oligodendrocytes by activating Erk1/2 in a calcium-dependent manner.
Animals
Animals, Newborn
Calcium
/ metabolism
Calcium Chelating Agents
/ pharmacology
Calcium Ionophores
/ pharmacology
Cells, Cultured
Cerebral Cortex
/ cytology
MAP Kinase Signaling System
/ drug effects
Mechanotransduction, Cellular
/ drug effects
Myelin Proteins
/ deficiency
Myelin Sheath
/ drug effects
Oligodendroglia
/ drug effects
Rats
Erk1/2
MBP
TBI
calcium
mechanotransduction
myelin
oligodendrocytes
Journal
Glia
ISSN: 1098-1136
Titre abrégé: Glia
Pays: United States
ID NLM: 8806785
Informations de publication
Date de publication:
10 2020
10 2020
Historique:
received:
05
06
2019
revised:
02
03
2020
accepted:
04
03
2020
pubmed:
15
3
2020
medline:
12
11
2021
entrez:
15
3
2020
Statut:
ppublish
Résumé
Myelin loss in the brain is a common occurrence in traumatic brain injury (TBI) that results from impact-induced acceleration forces to the head. Fast and abrupt head motions, either resulting from violent blows and/or jolts, cause rapid stretching of the brain tissue, and the long axons within the white matter tracts are especially vulnerable to such mechanical strain. Recent studies have shown that mechanotransduction plays an important role in regulating oligodendrocyte progenitors cell differentiation into oligodendrocytes. However, little is known about the impact of mechanical strain on mature oligodendrocytes and the stability of their associated myelin sheaths. We used an in vitro cellular stretch device to address these questions, as well as characterize a mechanotransduction mechanism that mediates oligodendrocyte responses. Mechanical stretch caused a transient and reversible myelin protein loss in oligodendrocytes. Cell death was not observed. Myelin protein loss was accompanied by an increase in intracellular Ca
Identifiants
pubmed: 32170885
doi: 10.1002/glia.23827
pmc: PMC7423729
mid: NIHMS1583684
doi:
Substances chimiques
Calcium Chelating Agents
0
Calcium Ionophores
0
Myelin Proteins
0
Calcium
SY7Q814VUP
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
2070-2085Subventions
Organisme : NIA NIH HHS
ID : R01 AG062475
Pays : United States
Organisme : NINDS NIH HHS
ID : R21 NS109708
Pays : United States
Informations de copyright
© 2020 Wiley Periodicals, Inc.
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