ArticleNeural regeneration research2013
Changes in secretory pathway Ca(2+)-ATPase 2 following focal cerebral ischemia/reperfusion injury.
Article in Neural regeneration research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- How cytosolic compartments play safeguard functions against neuroinflammation and cell death in cerebral ischemia.Metabolic brain disease · 2021Review
- Crosstalk among Calcium ATPases: PMCA, SERCA and SPCA in Mental Diseases.International journal of molecular sciences · 2021Review
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
This study aimed to investigate changes in secretory pathway Ca(2+)-ATPase 2 expression following cerebral ischemia/reperfusion injury, and to define the role of Ca(2+)-ATPases in oxidative stress. A rat model of cerebral ischemia/reperfusion injury was established using the unilateral middle cerebral artery occlusion method. Immunohistochemistry and reverse transcription-PCR assay results showed that compared with the control group, the expression of secretory pathway Ca(2+)-ATPase 2 protein and mRNA in the cerebral cortex and hippocampus of male rats did not significantly change during the ischemic period. However, secretory pathway Ca(2+)-ATPase 2 protein and mRNA expression reduced gradually at 1, 3, and 24 hours during the reperfusion period. Our experimental findings indicate that levels of secretory pathway Ca(2+)-ATPase 2 protein and mRNA expression in brain tissue change in response to cerebral ischemia/reperfusion injury.
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