Activation of GPER1 alleviates white matter injury by promoting microglia M2 polarization through EGFR/Stat3 pathway in intracerebral hemorrhage mice DOI Creative Commons
Xuyang Zhang, Jianchao Mao, Huanhuan Li

и другие.

Journal of Stroke and Cerebrovascular Diseases, Год журнала: 2025, Номер 34(6), С. 108315 - 108315

Опубликована: Апрель 12, 2025

White matter injury (WMI) is a major pathophysiological process after intracerebral hemorrhage (ICH). G protein-coupled estrogen receptor 1 (GPER1) has been validated to exert crucial role in regulating neuroinflammation and microglia polarization. Our previous report reveals activation of GPER1 improves the neurological deficits ICH via inhibition A1 astrocytes. However, on protection WMI modulation polarization remains unclear. In present study, mice model was induced by autologous whole blood injection vitro established treatment BV2 cells with FeSO4. Mice were treated agonist G1, antagonist G15 or EGFR inhibitor AG1478. Besides, conditional medium used intervene MO3.13 oligodendrocytes. Immunostaining, immunoblots, transmission electron microscope PI staining determine WMI, potential molecular mechanism ICH, respectively. data showed G1 ameliorated day 3 ICH. reduced release IL-1β, TNF-α increased produce IL-4, IL-10 as well shifting from proinflammatory M1 anti-inflammatory M2 phenotype vivo vitro. Meanwhile, alleviated oligodendrocytes death mitigating modulating Mechanistic study demonstrated EGFR/Stat3 signaling pathway involved Collectively, our findings through pathway.

Язык: Английский

Causal relations between immune cells and cerebral hemorrhage: a bidirectional Mendelian randomization study DOI
Zhimin Wu, Qiqi Wang, Z. Xiong

и другие.

International Journal of Neuroscience, Год журнала: 2025, Номер unknown, С. 1 - 14

Опубликована: Фев. 7, 2025

Previous studies have shown that an increased number of immune cells is closely associated with the onset and course changes intracerebral hemorrhage, but exact causal relationship has not been clarified. The aim this study was to investigate between hemorrhage by a two-way Mendelian randomization method. Two sets SNPs were used as instrumental variables analyses performed leave-one-out method assess validity heterogeneity included genetic variation instruments. level multiplicity variance instruments assessed. results showed clear three no related while scatterplot funnel plot confirmed causality less likely be biased; MR-Egger suggested pleiotropy found. Leave-one-out analysis applied suggest MR for single SNP robust; meanwhile, Meta-analysis combine two datasets, in fixed-effects model random-effects model, immunocyte CD66b on Granulocytic Myeloid-Derived Suppressor Cells other significantly causally test there significant difference different datasets. present found specific cell phenotypes analysis.

Язык: Английский

Процитировано

0
Activation of GPER1 alleviates white matter injury by promoting microglia M2 polarization through EGFR/Stat3 pathway in intracerebral hemorrhage mice DOI Creative Commons
Xuyang Zhang, Jianchao Mao, Huanhuan Li

и другие.

Journal of Stroke and Cerebrovascular Diseases, Год журнала: 2025, Номер 34(6), С. 108315 - 108315

Опубликована: Апрель 12, 2025

White matter injury (WMI) is a major pathophysiological process after intracerebral hemorrhage (ICH). G protein-coupled estrogen receptor 1 (GPER1) has been validated to exert crucial role in regulating neuroinflammation and microglia polarization. Our previous report reveals activation of GPER1 improves the neurological deficits ICH via inhibition A1 astrocytes. However, on protection WMI modulation polarization remains unclear. In present study, mice model was induced by autologous whole blood injection vitro established treatment BV2 cells with FeSO4. Mice were treated agonist G1, antagonist G15 or EGFR inhibitor AG1478. Besides, conditional medium used intervene MO3.13 oligodendrocytes. Immunostaining, immunoblots, transmission electron microscope PI staining determine WMI, potential molecular mechanism ICH, respectively. data showed G1 ameliorated day 3 ICH. reduced release IL-1β, TNF-α increased produce IL-4, IL-10 as well shifting from proinflammatory M1 anti-inflammatory M2 phenotype vivo vitro. Meanwhile, alleviated oligodendrocytes death mitigating modulating Mechanistic study demonstrated EGFR/Stat3 signaling pathway involved Collectively, our findings through pathway.

Язык: Английский

Процитировано

0