Cofilin-actin rod formation in neuronal processes after brain ischemia.
Functional impairment after brain ischemia results in part from loss of neuronal spines and dendrites, independent of neuronal death. Cofilin-actin rods are covalently linked aggregates of cofilin-1 and actin that form in neuronal processes (neurites) under conditions of ATP depletion and oxidative...
| Main Authors: | , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2018-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC6191105?pdf=render |
| _version_ | 1818209665701380096 |
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| author | Seok Joon Won Angela M Minnella Long Wu Claire H Eun Eric Rome Paco S Herson Alisa E Shaw James R Bamburg Raymond A Swanson |
| author_facet | Seok Joon Won Angela M Minnella Long Wu Claire H Eun Eric Rome Paco S Herson Alisa E Shaw James R Bamburg Raymond A Swanson |
| author_sort | Seok Joon Won |
| collection | DOAJ |
| description | Functional impairment after brain ischemia results in part from loss of neuronal spines and dendrites, independent of neuronal death. Cofilin-actin rods are covalently linked aggregates of cofilin-1 and actin that form in neuronal processes (neurites) under conditions of ATP depletion and oxidative stress, and which cause neurite degeneration if not disassembled. ATP depletion and oxidative stress occur with differing severity, duration, and time course in different ischemic conditions. Here we evaluated four mouse models of brain ischemia to define the conditions that drive formation of cofilin-actin rods. Three of the models provide early reperfusion: transient middle cerebral artery occlusion (MCAo), transient bilateral common carotid artery occlusion (CCAo), and cardiac arrest / cardiopulmonary resuscitation (CA/CPR). Early reperfusion restores ATP generating capacity, but also induces oxidative stress. The fourth model, photothrombotic cortical infarction, does not provide reperfusion. Cofilin-actin rods were formed in each of these models, but with differing patterns. Where acute reperfusion occurred, rod formation was maximal within 4 hours after reperfusion. Where infarction occurred, rods continued to form for at least 24 hours after ischemic onset, and extended into the adjacent non-ischemic tissue. Interventions that limit cofilin-actin rod formation may help to preserve integrity of neuronal processes in permanent ischemia. |
| first_indexed | 2024-12-12T05:04:20Z |
| format | Article |
| id | doaj.art-6e01d2d297074ff19f65214cf4fde775 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-12T05:04:20Z |
| publishDate | 2018-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-6e01d2d297074ff19f65214cf4fde7752022-12-22T00:37:09ZengPublic Library of Science (PLoS)PLoS ONE1932-62032018-01-011310e019870910.1371/journal.pone.0198709Cofilin-actin rod formation in neuronal processes after brain ischemia.Seok Joon WonAngela M MinnellaLong WuClaire H EunEric RomePaco S HersonAlisa E ShawJames R BamburgRaymond A SwansonFunctional impairment after brain ischemia results in part from loss of neuronal spines and dendrites, independent of neuronal death. Cofilin-actin rods are covalently linked aggregates of cofilin-1 and actin that form in neuronal processes (neurites) under conditions of ATP depletion and oxidative stress, and which cause neurite degeneration if not disassembled. ATP depletion and oxidative stress occur with differing severity, duration, and time course in different ischemic conditions. Here we evaluated four mouse models of brain ischemia to define the conditions that drive formation of cofilin-actin rods. Three of the models provide early reperfusion: transient middle cerebral artery occlusion (MCAo), transient bilateral common carotid artery occlusion (CCAo), and cardiac arrest / cardiopulmonary resuscitation (CA/CPR). Early reperfusion restores ATP generating capacity, but also induces oxidative stress. The fourth model, photothrombotic cortical infarction, does not provide reperfusion. Cofilin-actin rods were formed in each of these models, but with differing patterns. Where acute reperfusion occurred, rod formation was maximal within 4 hours after reperfusion. Where infarction occurred, rods continued to form for at least 24 hours after ischemic onset, and extended into the adjacent non-ischemic tissue. Interventions that limit cofilin-actin rod formation may help to preserve integrity of neuronal processes in permanent ischemia.http://europepmc.org/articles/PMC6191105?pdf=render |
| spellingShingle | Seok Joon Won Angela M Minnella Long Wu Claire H Eun Eric Rome Paco S Herson Alisa E Shaw James R Bamburg Raymond A Swanson Cofilin-actin rod formation in neuronal processes after brain ischemia. PLoS ONE |
| title | Cofilin-actin rod formation in neuronal processes after brain ischemia. |
| title_full | Cofilin-actin rod formation in neuronal processes after brain ischemia. |
| title_fullStr | Cofilin-actin rod formation in neuronal processes after brain ischemia. |
| title_full_unstemmed | Cofilin-actin rod formation in neuronal processes after brain ischemia. |
| title_short | Cofilin-actin rod formation in neuronal processes after brain ischemia. |
| title_sort | cofilin actin rod formation in neuronal processes after brain ischemia |
| url | http://europepmc.org/articles/PMC6191105?pdf=render |
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