About: Stimulator of IFN genes mediates neuroinflammatory injury by suppressing AMPK signal in experimental subarachnoid hemorrhage

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About: Stimulator of IFN genes mediates neuroinflammatory injury by suppressing AMPK signal in experimental subarachnoid hemorrhage Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Stimulator of IFN genes mediates neuroinflammatory injury by suppressing AMPK signal in experimental subarachnoid hemorrhage
Creator	Cao, Yang Zhou, Hang Yan, Feng Cao, Shenglong Chen, Gao Chen, Huaijun Chen, Jingyin Fu, Xiongjie Gu, Chi Li, Jianru Peng, Yucong Xu, Chaoran Xu, Hangzhe Ying, Guangyu Zeng, Hanhai Zhuang, Jianfeng
Source	Medline; PMC
abstract	BACKGROUND: Neuroinflammation is closely associated with the poor prognosis in subarachnoid hemorrhage (SAH) patients. This study was aimed to determine the role of stimulator of IFN genes (STING), an essential regulator to innate immunity, in the context of SAH. METHODS: A total of 344 male C57BL/6 J mice were subjected to endovascular perforation to develop a model of SAH. Selective STING antagonist C-176 and STING agonist CMA were administered at 30 min or 1 h post-modeling separately. To investigate the underlying mechanism, the AMPK inhibitor compound C was administered intracerebroventricularly at 30 min before surgery. Post-SAH assessments included SAH grade, neurological test, brain water content, western blotting, RT-PCR, and immunofluorescence. Oxygenated hemoglobin was introduced into BV2 cells to establish a SAH model in vitro. RESULTS: STING was mainly distributed in microglia, and microglial STING expression was significantly increased after SAH. Administration of C-176 substantially attenuated SAH-induced brain edema and neuronal injury. More importantly, C-176 significantly alleviated both short-term and persistent neurological dysfunction after SAH. Meanwhile, STING agonist CMA remarkably exacerbated neuronal injury and deteriorated neurological impairments. Mechanically, STING activation aggravated neuroinflammation via promoting microglial activation and polarizing into M1 phenotype, evidenced by microglial morphological changes, as well as the increased level of microglial M1 markers including IL-1β, iNOS, IL-6, TNF-α, MCP-1, and NLRP3 inflammasome, while C-176 conferred a robust anti-inflammatory effect. However, all the mentioned beneficial effects of C-176 including alleviated neuroinflammation, attenuated neuronal injury and the improved neurological function were reversed by AMPK inhibitor compound C. Meanwhile, the critical role of AMPK signal in C-176 mediated anti-inflammatory effect was also confirmed in vitro. CONCLUSION: Microglial STING yielded neuroinflammation after SAH, while pharmacologic inhibition of STING could attenuate SAH-induced inflammatory injury at least partly by activating AMPK signal. These data supported the notion that STING might be a potential therapeutic target for SAH.
has issue date	2020-05-25(xsd:dateTime)
bibo:doi	10.1186/s12974-020-01830-4
bibo:pmid	32450897
has license	cc-by
sha1sum (hex)	4767595e3f60b1b5649fa7d936b4bd5cca1f51e4
schema:url	https://doi.org/10.1186/s12974-020-01830-4
resource representing a document's title	Stimulator of IFN genes mediates neuroinflammatory injury by suppressing AMPK signal in experimental subarachnoid hemorrhage
has PubMed Central identifier	PMC7247752
has PubMed identifier	32450897
schema:publication	J Neuroinflammation
resource representing a document's body	covid:4767595e3f60b1b5649fa7d936b4bd5cca1f51e4#body_text
is schema:about of	named entity 'Neuroinflammation' named entity 'subarachnoid hemorrhage' named entity 'innate immunity' named entity 'STING' named entity 'Stimulator' named entity 'subarachnoid hemorrhage' named entity 'NLRP3' named entity '1:200' named entity 'Sigma-Aldrich' named entity 'Interferon regulatory factor 3' named entity 'neurological dysfunction' named entity 'alcohol' named entity 'phenotype' named entity 'iNOS' named entity 'astrocytes' named entity 'internal control' named entity 'streptomycin' named entity 'phenotype' named entity 'TBK1' named entity 'cyclic GMP-AMP' named entity 'cresyl violet' named entity 'mammary tumors' named entity 'SAH' named entity 'microglia' named entity 'TBK1' named entity 'neural regeneration' named entity '28 days' named entity 'SAH' named entity 'antiinflammatory' named entity 'AMPK' named entity 'pathological process' named entity '49, 50' named entity 'neurons' named entity 'immune cell' named entity 'burr hole' named entity 'AMPK' named entity 'transcription factor IRF3' named entity 'therapeutic strategies' named entity 'neurological dysfunction' named entity 'pro-IL-1β' named entity 'neurological dysfunction' named entity 'PBS' named entity 'cytosolic DNA sensor' named entity 'hippocampus' named entity 'IL-10' named entity 'SAH' named entity 'soma' named entity 'colitis' named entity 'blood glucose levels' named entity 'mice' named entity 'phosphorylation' named entity 'phenotype' named entity 'microphotographs' named entity 'phenotype' named entity 'western blotting' named entity 'dsDNA' named entity 'bacteria' named entity 'traumatic brain injury' named entity 'CD16' named entity 'lipid oxidation' named entity 'critical role' named entity 'brain injury' named entity 'macrophages' named entity 'infection' named entity 'SAH' named entity 'protein'

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