ArticleInflammation2019
Protective Effect of Mitogen- and Stress-Activated Protein Kinase on the Rats with Focal Ischemia-Reperfusion Injury.
Article in Inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.
What it found
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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, 1 citations in OpenAlex.
- Neuroinflammation promotes the development of pharmacoresistant epilepsy by triggering the MSK1/CREB signaling pathway.Scientific reports · 2026Article
- Protective Effects of Ischemic Postconditioning on Livers in Rats with Limb Ischemia-Reperfusion via Glycogen Synthase Kinase 3 beta (GSK-3β)/Fyn/Nuclear Receptor-Erythroid-2-Related Factor (Nrf2) Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitogen- and stress-activated protein kinase (MSK) is a recently identified nuclear cAMP-regulated enhancer B (CREB) and histone H3 kinase that responds to both mitogen- and stress-activated protein kinases. This study was designed to investigate the protective effect of MSK on the rats with focal ischemia-reperfusion injury. The rat model was established by inserting thread into the middle cerebral artery. The protein expression was measured by immunoblotting. The localization of MSK was measured by immunofluorescence assay. Highly-differentiated pheochromocytoma 12 (PC12) is used as a sympathetic neuron-like cell line and treated with glutamate to induce neurotoxicity. MSK was knocked down and overexpressed by siRNA and MSK over-expressing vector, respectively. The cell viability was measured by cell counting kit (CCK-8) assay. The coronal sections were isolated and stained with 2, 3, 5-triphenyltetrazolium chloride (TTC) to determine infarct volume. Finally, astrocytes were separated from cerebral cortexes of normal rats to analyze the effects of MSK on inflammatory response. In the rats with focal ischemia-reperfusion injury, the expression of MSK was reduced, reaching the lowest level at 3 d after ischemia-reperfusion, and then recovered gradually. MSK was found mainly localized in neurons and astrocytes. The expression levels of caspase-3, caspase-8, caspase-9, and INOS showed the opposite trend with respect to MSK. Further analysis showed that overexpression of MSK exerted a protective effect on glutamate-induced neurotoxicity through inhibiting apoptosis of PC12 cells, as well as decreased the infarct size in rat with focal ischemia-reperfusion injury. On the contrary, knockdown of MSK showed opposite results. Finally, MSK suppressed LPS-induced inflammatory response by decreasing the expression of inducible nitric oxide synthase (INOS) and increasing the expression of interleukin-10 (IL-10) in astrocytes from cerebral cortexes of normal rats. In conclusion, MSK exerted a protective effect on rat with focal ischemia-reperfusion injury through its anti-apoptotic effect on neurons and anti-inflammatory effect on astrocytes.
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