ArticleNeurochemical research2021
Spata2 Knockdown Exacerbates Brain Inflammation via NF-κB/P38MAPK Signaling and NLRP3 Inflammasome Activation in Cerebral Ischemia/Reperfusion Rats.
Article in Neurochemical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- A single-cell genomic atlas for the effects of chronic ethanol exposure in the mouse dorsal striatum.Molecular psychiatry · 2025Article
- Clinical and functional significance of SPATA2 in cancer particularly in LIHC.Scientific reports · 2025Article
- Role of CYLD in brain physiology and pathology.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Investigation of the effects ofFrontiers in pharmacology · 2024Article
- Aging-related genes revealed Neuroinflammatory mechanisms in ischemic stroke by bioinformatics.Heliyon · 2023Article
- Pre exposure to enriched environment alleviates brain injury after ischemia-reperfusion by inhibiting p38MAPK/STAT1 pathway.Molecular biology reports · 2023Article
- Calycosin protects against chronic prostatitis in rats via inhibition of the p38MAPK/NF-κB pathway.Open medicine (Warsaw, Poland) · 2023Article
- The effect of triple reuptake inhibitor toludesvenlafaxine on neurological function in cerebral ischemic rats.Frontiers in pharmacology · 2023Article
- Identification of a miRNA-mRNA regulatory network for post-stroke depression: a machine-learning approach.Frontiers in neurology · 2023Article
- The role of SPATA2 in TNF signaling, cancer, and spermatogenesis.Cell death & disease · 2022Review
- NLRP3: Role in ischemia/reperfusion injuries.Frontiers in immunology · 2022Review
- Multiple Roles of Paeoniflorin in Alzheimer's Disease.Evidence-based complementary and alternative medicine : eCAM · 2022Review
- Hispidin inhibits LPS-induced nitric oxide production in BV-2 microglial cells via ROS-dependent MAPK signaling.Experimental and therapeutic medicine · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Brain inflammation induced by ischemic stroke is an important cause of secondary brain injury. The nuclear factor kappa B (NF-κB), mitogen-activated protein kinase (MAPK), and NLRP3 inflammasome signaling are believed to drive the progression of brain inflammation. Spermatogenesis-associated protein2 (SPATA2) functions as a partner protein that recruits CYLD, a negative regulator of NF-κB signaling, to signaling complexes. However, the role of SPATA2 in the central nervous system remains unclear and whether it is involved in regulating inflammatory responses remains controversial. Rats were subjected to transient middle cerebral artery occlusion followed by reperfusion (tMCAO/R) surgery. The expression and localization of SPATA2 in the brain were investigated. The lentivirus-mediated shRNA was employed to inhibit SPATA2 expression. The inflammatory responses and outcomes of Spata2 knockdown were investigated. SPATA2 was co-localized with CYLD in neurons. SPATA2 expression was reduced in tMCAO/R rats. Spata2 knockdown resulted in increased microglia, increased expression of Tnfa, Il-1β, and Il-18, decreased Garcia score, and increased infarct volume. Spata2 knockdown resulted in the activation of P38MAPK and NLRP3 inflammasome and the increased activation of NF-κB signaling. These results suggest that SPATA2 plays a protective role against brain inflammation induced by ischemia/reperfusion injury. Therefore, SPATA2 could be a potential therapeutic target for treating ischemic stroke.
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