ArticleCNS neuroscience & therapeutics2022
Role of Rph3A in brain injury induced by experimental cerebral ischemia-reperfusion model in rats.
Article in CNS neuroscience & therapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 22 citations in OpenAlex.
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- The choroidal nervous system: a link between mineralocorticoid receptor and pachychoroid.Acta neuropathologica · 2023Article
- Identification and Experimental Validation of Parkinson's Disease with Major Depressive Disorder Common Genes.Molecular neurobiology · 2023Article
- Presynaptic Congenital Myasthenic Syndromes: Understanding Clinical Phenotypes through In vivo Models.Journal of neuromuscular diseases · 2023Review
- Different gender-derived gut microbiota influence stroke outcomes by mitigating inflammation.Journal of neuroinflammation · 2022Article
- A Metabolic Plasticity-Based Signature for Molecular Classification and Prognosis of Lower-Grade Glioma.Brain sciences · 2022Article
- Role of Rph3A in brain injury induced by experimental cerebral ischemia-reperfusion model in rats.CNS neuroscience & therapeutics · 2022Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimThe aim was to study the role of Rph3A in neuronal injury induced by cerebral ischemia-reperfusion.
methodsThe protein and mRNA levels of Rph3A in penumbra were detected by Western blot. The localization of Rph3A in different cell types in penumbra was detected by immunofluorescence. Apoptosis in the brain was detected by TUNEL staining. We tested neurobehavioral evaluation using rotarod test, adhesive-removal test, and Morris Water maze test. We examined the expression and localization of Rph3A in cultured neurons and astrocytes in vitro by Western blot and ELISA, respectively.
resultsThe mRNA and protein levels of Rph3A had significantly increased in brain penumbra of the rat MCAO/R model. Rph3A was mainly distributed in neurons and astrocytes and was significantly increased by MCAO/R. We downregulated Rph3A and found that it further worsened the cerebral infarct, neuronal death and behavioral, cognitive, and memory impairments in rats after MCAO/R. We also found that ischemia-reperfusion upregulated the in vitro protein level and secretion of Rph3A in astrocytes but led to a decrease in the protein level of Rph3A in neurons.
conclusionThe increase in Rph3A in the brain penumbra may be an endogenous protective mechanism against ischemia-reperfusion injury, which is mainly dominated by astrocytes.
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