ArticleExperimental and therapeutic medicine2021
MSK1 downregulation is involved in inflammatory responses following subarachnoid hemorrhage in rats.
Article in Experimental and therapeutic medicine, 2021. 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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2 citing papers in PubMed, 3 citations in OpenAlex.
- Cigarette smoking induces NLRP3 inflammasome activation in patients with atrial fibrillation.American journal of physiology. Heart and circulatory physiology · 2025Article
- HOXC6 drives a therapeutically targetable pancreatic cancer growth and metastasis pathway by regulating MSK1 and PPP2R2B.Cell reports. Medicine · 2023Article
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Authors and funding
8 authors at 7 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Subarachnoid hemorrhage (SAH) is a life-threatening neurological disease. Recently, inflammatory factors have been confirmed to be responsible for the brain damage associated with SAH. Therefore, studying the post-SAH inflammatory reaction may clarify the mechanism of SAH. Mitogen and stress-activated protein kinase 1 (MSK1) causes the phosphorylation of NF-κB and regulates the activity of pro-inflammatory transcription factors. The present study aimed to identify the potential role of MSK1 in inflammation and brain damage development following SAH. A cisterna magna blood injection model was established in Sprague-Dawley rats. Hematoxylin and eosin staining, reverse transcription-quantitative polymerase chain reaction assays and double immunofluorescence staining were used to analyze the role of MSK1, IL-1β and TNF-α in the inflammatory process after SAH. In a model of lipopolysaccharide-induced astrocyte inflammation, the effect of overexpressing MSK1 overexpression was analyzed by western blot analysis. The results demonstrated that MSK1 expression were negatively correlated with TNF-α and IL-1β expression levels, and reached peak levels 2 days after TNF-α and IL-1β. The double immunofluorescence staining results showed that the expression of MSK1 was in the same plane of view as TNF-α and IL-1β in the brain cortex. Furthermore, the
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