ArticleJournal of neurochemistry2021
Activation of neuronal Ras-related C3 botulinum toxin substrate 1 (Rac1) improves post-stroke recovery and axonal plasticity in mice.
Article in Journal of neurochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- White matter injury after brain ischemia.Experimental neurology · 2026Review
- Temporal and Spatial Gene Expression Dynamics in Neonatal HI Hippocampus with Focus on Arginase.Cells · 2026Article
- Integrated bioinformatics analysis and biological experiments to identify key immune genes in vascular dementia.Frontiers in immunology · 2025Article
- Activation of cerebral Ras-related C3 botulinum toxin substrate (Rac) 1 promotes post-ischemic stroke functional recovery in aged mice.Neural regeneration research · 2024Article
- Ginsenoside Rg1 promotes neurite growth of retinal ganglion cells through cAMP/PKA/CREB pathways.Journal of ginseng research · 2024Article
- Knockdown of Porf-2 restores visual function after optic nerve crush injury.Cell death & disease · 2023Article
- PAK1 contributes to cerebral ischemia/reperfusion injury by regulating the blood-brain barrier integrity.iScience · 2023Article
- Overexpression of mitogen-activated protein kinase phosphatase-1 in endothelial cells reduces blood-brain barrier injury in a mouse model of ischemic stroke.Neural regeneration research · 2023Article
- NLRP3 inflammasome activation increases brain oxidative stress after transient global cerebral ischemia in rats.The International journal of neuroscience · 2023Article
- Reverse effects ofFrontiers in cellular and infection microbiology · 2022Article
- Non-invasive Vagus Nerve Stimulation in Cerebral Stroke: Current Status and Future Perspectives.Frontiers in neuroscience · 2022Review
- Activation of creER recombinase in the mouse calvaria induces local recombination without effects on distant skeletal segments.Scientific reports · 2021Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Long-term disability after stroke is common but the mechanisms of post-stroke recovery remain unclear. Cerebral Ras-related C3 botulinum toxin substrate (Rac) 1 contributes to functional recovery after ischemic stroke in mice. As Rac1 plays divergent roles in individual cell types after central neural system injury, we herein examined the specific role of neuronal Rac1 in post-stroke recovery and axonal regeneration. Young male mice were subjected to 60-min of middle cerebral artery occlusion (MCAO). Inducible deletion of neuronal Rac1 by daily intraperitoneal injection of tamoxifen (2 mg/40 g) into Thy1-creER/Rac1-floxed mice day 7-11 after MCAO worsened cognitive (assayed by novel object recognition test) and sensorimotor (assayed by adhesive removal and pellet reaching tests) recovery day 14-28 accompanied with the reduction of neurofilament-L (NFL) and myelin basic protein (MBP) and the elevation of glial fibrillary acidic protein (GFAP) in the peri-infarct zone assessed by immunostaining. Whereas the brain tissue loss was not altered assayed by cresyl violet staining. In another approach, delayed overexpression of neuronal Rac1 by injection of lentivirus encoding Rac1 with neuronal promotor into both the cortex and striatum (total 4 μl at 1 × 10
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