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Mechanism of Stat1 in the neuronal Ca 2+ overload after intracerebral hemorrhage via the H3K27ac/Trpm7 axis
Journal of neurophysiology, 2022-07, Vol.128 (1), p.253-262
[Peer Reviewed Journal]
ISSN: 0022-3077 ;EISSN: 1522-1598 ;DOI: 10.1152/jn.00083.2022 ;PMID: 35642851
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Title:
Mechanism of Stat1 in the neuronal Ca 2+ overload after intracerebral hemorrhage via the H3K27ac/Trpm7 axis
Author:
Li, Jialin
;
Ren, Hecheng
;
Wang, Yanbing
;
Hoang, Dung Minh
;
Li, Yongsheng
;
Yao, Xiuhua
Is Part Of:
Journal of neurophysiology, 2022-07, Vol.128 (1), p.253-262
Description:
Intracerebral hemorrhage (ICH) is classified as a subtype of stroke and Calcium (Ca ) overload is a catalyst for ICH. This study explored the mechanisms of Stat1 (signal transducer and activator of transcription 1) in the neuronal Ca overload after ICH. ICH mouse models and in vitro cell models were established. Stat1 and transient receptor potential melastatin 7 (Trpm7) were detected up-regulated in ICH models. Afterwards, the mice were infected with the lentivirus containing sh-Stat1, and HT22 cells were treated with si-Stat1 and the lentivirus containing pcDNA3.1-Trpm7. The neurologic functional impairment, histopathological damage, and Nissl body in mice were all measured. HT22 cell viability and apoptosis were identified. The levels of Ca , Trpm7 mRNA, H3K27 acetylation (H3K27ac), CaMKII-α, and p-Stat1 protein in the tissues and cells were determined. We found that silencing Stat1 alleviated ICH damage and repressed the neuronal Ca overload after ICH. H3K27ac enrichment in the Trpm7 promoter region was examined and we found that p-Stat1 accelerated Trpm7 transcription via promoting H3K27ac in the Trpm7 promoter region. Besides, Trpm7 overexpression increased Ca overload and aggravated ICH. Overall, p-Stat1 promoted Trpm7 transcription and further aggravated the Ca overload after ICH.
Publisher:
United States
Language:
English
Identifier:
ISSN: 0022-3077
EISSN: 1522-1598
DOI: 10.1152/jn.00083.2022
PMID: 35642851
Source:
Alma/SFX Local Collection
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