In:
PLOS Biology, Public Library of Science (PLoS), Vol. 19, No. 12 ( 2021-12-13), p. e3001399-
Abstract:
Ischemic stroke is a major cause of death and long-term disability. We demonstrate that middle cerebral artery occlusion (MCAO) in mice leads to a strong decline in dendritic arborization of penumbral neurons. These defects were subsequently repaired by an ipsilateral recovery process requiring the actin nucleator Cobl. Ischemic stroke and excitotoxicity, caused by calpain-mediated proteolysis, significantly reduced Cobl levels. In an apparently unique manner among excitotoxicity-affected proteins, this Cobl decline was rapidly restored by increased mRNA expression and Cobl then played a pivotal role in poststroke dendritic arbor repair in peri-infarct areas. In Cobl knockout (KO) mice, the dendritic repair window determined to span day 2 to 4 poststroke in wild-type (WT) strikingly passed without any dendritic regrowth. Instead, Cobl KO penumbral neurons of the primary motor cortex continued to show the dendritic impairments caused by stroke. Our results thereby highlight a powerful poststroke recovery process and identified causal molecular mechanisms critical during poststroke repair.
Type of Medium:
Online Resource
ISSN:
1545-7885
DOI:
10.1371/journal.pbio.3001399
DOI:
10.1371/journal.pbio.3001399.g001
DOI:
10.1371/journal.pbio.3001399.g002
DOI:
10.1371/journal.pbio.3001399.g003
DOI:
10.1371/journal.pbio.3001399.g004
DOI:
10.1371/journal.pbio.3001399.g005
DOI:
10.1371/journal.pbio.3001399.g006
DOI:
10.1371/journal.pbio.3001399.g007
DOI:
10.1371/journal.pbio.3001399.t001
DOI:
10.1371/journal.pbio.3001399.s001
DOI:
10.1371/journal.pbio.3001399.s002
DOI:
10.1371/journal.pbio.3001399.s003
DOI:
10.1371/journal.pbio.3001399.s004
DOI:
10.1371/journal.pbio.3001399.s005
DOI:
10.1371/journal.pbio.3001399.s006
DOI:
10.1371/journal.pbio.3001399.s007
DOI:
10.1371/journal.pbio.3001399.s008
DOI:
10.1371/journal.pbio.3001399.s009
DOI:
10.1371/journal.pbio.3001399.s010
DOI:
10.1371/journal.pbio.3001399.s011
DOI:
10.1371/journal.pbio.3001399.s012
DOI:
10.1371/journal.pbio.3001399.s013
DOI:
10.1371/journal.pbio.3001399.s014
DOI:
10.1371/journal.pbio.3001399.s015
DOI:
10.1371/journal.pbio.3001399.s016
DOI:
10.1371/journal.pbio.3001399.s017
DOI:
10.1371/journal.pbio.3001399.s018
DOI:
10.1371/journal.pbio.3001399.s019
DOI:
10.1371/journal.pbio.3001399.s020
DOI:
10.1371/journal.pbio.3001399.s021
DOI:
10.1371/journal.pbio.3001399.s022
DOI:
10.1371/journal.pbio.3001399.s023
DOI:
10.1371/journal.pbio.3001399.s024
DOI:
10.1371/journal.pbio.3001399.s025
DOI:
10.1371/journal.pbio.3001399.r001
DOI:
10.1371/journal.pbio.3001399.r002
DOI:
10.1371/journal.pbio.3001399.r003
DOI:
10.1371/journal.pbio.3001399.r004
DOI:
10.1371/journal.pbio.3001399.r005
DOI:
10.1371/journal.pbio.3001399.r006
DOI:
10.1371/journal.pbio.3001399.r007
Language:
English
Publisher:
Public Library of Science (PLoS)
Publication Date:
2021
detail.hit.zdb_id:
2126773-X
Permalink