ArticleFrontiers in cellular neuroscience2022
Casein kinase 2 attenuates brain injury induced by intracerebral hemorrhage via regulation of NR2B phosphorylation.
Article in Frontiers in cellular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 11 citations in OpenAlex.
- CSNK2B gene replacement rescues autism-related phenotypes and establishes translational EEG biomarkers.Cell reports. Medicine · 2026Article
- UBL4A as a suppressor of intracerebral hemorrhage by binding to MAPK14 and promoting MAPK14 ubiquitination.Genes & genomics · 2026Article
- NDRG4 overexpression is associated with reduced apoptosis after intracerebral hemorrhage via the PI3K/Akt/GSK3β signaling pathway.Scientific reports · 2026Article
- From bench to bedside: nanomedicine development for intracerebral hemorrhage - exploring microenvironment, innovation, and translation.Journal of nanobiotechnology · 2025Review
- Claudin-2 upregulation enhances intestinal permeability, immune activation, dysbiosis, and mortality in sepsis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Astrocyte Regulation of Neuronal Function and Survival in Stroke Pathophysiology.Advances in neurobiology · 2024Review
- Astrocytes in intracerebral hemorrhage: impact and therapeutic objectives.Frontiers in molecular neuroscience · 2024Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Intracerebral hemorrhage (ICH) is a common cerebrovascular disease with high incidence, disability, and mortality. Casein kinase 2 (CK2) is a serine/threonine kinase with hundreds of identified substrates and plays an important role in many diseases. This study aimed to explore whether CK2 plays protective roles in ICH-induced neuronal apoptosis, inflammation, and oxidative stress through regulation NR2B phosphorylation. Methods: CK2 expression level of brain tissues taken from ICH patients was determined by immunoblotting. Neurons from embryonic rat and astrocytes from newborn rats were cultured and treated by Hemoglobin chloride (Hemin). The proliferation of astrocytes, the apoptosis and oxidative stress of neurons and the inflammatory factors of astrocytes were detected. CK2 expression was determined in ICH model rats. The effects of CK2 overexpression plasmid (pc-CK2) on neurobehavioral defects and brain water content in ICH rats were observed. Results: CK2 expression in ICH patients was down-regulated. Overexpression of CK2 promoted the astrocyte proliferation, inhibited neuronal apoptosis, and reduced astrocyte-mediated inflammation. Conclusion: CK2 phosphorylated NR2B, down-regulated the expression of NR2B, interfered with the interaction between NR2B and PSD95, alleviated inflammatory reactions, inhibited neuronal apoptosis and oxidative stress after ICH. CK2 and NR2B may be new potential therapeutic targets for the treatment of ICH. However, the limitation of this study is that we only investigated the regulation of NR2B by CK2.
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