Poststroke dendritic arbor regrowth requires the actin nucleator Cobl
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...
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| Veröffentlicht in: | PLoS biology 2021-12, Vol.19 (12), p.e3001399-e3001399 |
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| creator | Ji, Yuanyuan Koch, Dennis González Delgado, Jule Günther, Madlen Witte, Otto W Kessels, Michael M Frahm, Christiane Qualmann, Britta |
| description | 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. |
| doi_str_mv | 10.1371/journal.pbio.3001399 |
| format | Article |
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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.</description><identifier>ISSN: 1545-7885</identifier><identifier>ISSN: 1544-9173</identifier><identifier>EISSN: 1545-7885</identifier><identifier>DOI: 10.1371/journal.pbio.3001399</identifier><identifier>PMID: 34898601</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Actin ; Actin Cytoskeleton - metabolism ; Actins - metabolism ; Analysis ; Animals ; Biology and Life Sciences ; Brain ; Calpain ; Cerebral blood flow ; Cortex (motor) ; Cytoskeletal Proteins - metabolism ; Dendritic branching ; Dendritic cells ; Dendritic structure ; Excitotoxicity ; Gene expression ; Gene Expression - genetics ; Genetic aspects ; Identification and classification ; Infarction, Middle Cerebral Artery ; Ischemia ; Ischemic Stroke - metabolism ; Male ; Medicine and Health Sciences ; Messenger RNA ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Microfilament Proteins - genetics ; Microfilament Proteins - metabolism ; Microfilament Proteins - physiology ; Molecular modelling ; Neuronal Plasticity - physiology ; Neurons ; Neurons - metabolism ; Neurons - physiology ; Occlusion ; Properties ; Proteins ; Proteolysis ; Recovery ; Regrowth ; Repair ; Research and Analysis Methods ; Stroke ; Stroke (Disease)</subject><ispartof>PLoS biology, 2021-12, Vol.19 (12), p.e3001399-e3001399</ispartof><rights>COPYRIGHT 2021 Public Library of Science</rights><rights>2021 Ji et al. 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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.</description><subject>Actin</subject><subject>Actin Cytoskeleton - metabolism</subject><subject>Actins - metabolism</subject><subject>Analysis</subject><subject>Animals</subject><subject>Biology and Life Sciences</subject><subject>Brain</subject><subject>Calpain</subject><subject>Cerebral blood flow</subject><subject>Cortex (motor)</subject><subject>Cytoskeletal Proteins - metabolism</subject><subject>Dendritic branching</subject><subject>Dendritic cells</subject><subject>Dendritic structure</subject><subject>Excitotoxicity</subject><subject>Gene expression</subject><subject>Gene Expression - genetics</subject><subject>Genetic aspects</subject><subject>Identification and classification</subject><subject>Infarction, Middle Cerebral Artery</subject><subject>Ischemia</subject><subject>Ischemic Stroke - metabolism</subject><subject>Male</subject><subject>Medicine and Health Sciences</subject><subject>Messenger RNA</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Microfilament Proteins - 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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.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>34898601</pmid><doi>10.1371/journal.pbio.3001399</doi><orcidid>https://orcid.org/0000-0002-8114-8212</orcidid><orcidid>https://orcid.org/0000-0002-5743-5764</orcidid><orcidid>https://orcid.org/0000-0003-2101-4105</orcidid><orcidid>https://orcid.org/0000-0001-5967-0744</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Actin Actin Cytoskeleton - metabolism Actins - metabolism Analysis Animals Biology and Life Sciences Brain Calpain Cerebral blood flow Cortex (motor) Cytoskeletal Proteins - metabolism Dendritic branching Dendritic cells Dendritic structure Excitotoxicity Gene expression Gene Expression - genetics Genetic aspects Identification and classification Infarction, Middle Cerebral Artery Ischemia Ischemic Stroke - metabolism Male Medicine and Health Sciences Messenger RNA Mice Mice, Inbred C57BL Mice, Knockout Microfilament Proteins - genetics Microfilament Proteins - metabolism Microfilament Proteins - physiology Molecular modelling Neuronal Plasticity - physiology Neurons Neurons - metabolism Neurons - physiology Occlusion Properties Proteins Proteolysis Recovery Regrowth Repair Research and Analysis Methods Stroke Stroke (Disease) |
| title | Poststroke dendritic arbor regrowth requires the actin nucleator Cobl |
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