FCGR1A Alleviates Ischemic Stroke-induced Injury by Promoting Anti-Inflammatory Microglial Polarization via the AMPK–mTOR Signaling Pathway DOI Creative Commons
Meng Liu,

Xiang‐Bing Fan,

D Chen

и другие.

Frontiers in Bioscience-Landmark, Год журнала: 2025, Номер 30(5)

Опубликована: Апрель 29, 2025

Background: Ischemic stroke triggers inflammatory responses that lead to neuronal damage, with microglial polarization significantly influencing post-stroke inflammation. This study explores the role of Fc gamma receptor Ia (FCGR1A) in and its regulatory mechanisms ischemic stroke. Methods: Differentially expressed genes (DEGs) associated were identified using GSE58294 dataset. Hub found by analyzing protein–protein interaction (PPI) networks. BV2 microglia subjected oxygen–glucose deprivation/reoxygenation (OGD/R) mimic conditions vitro, FCGR1A marker levels assessed. Besides, cells stimulated lipopolysaccharide (LPS) interferon-gamma (IFN-γ) induce M1 polarization, effects overexpression knockdown on cytokine production evaluated. The function AMP-activated protein kinase (AMPK)-mTOR pathway regulating was further investigated mTOR inhibitor rapamycin (RAP). Results: From 327 DEGs identified, chosen as a hub gene. OGD/R treatment produced time-dependent rise FCGR1A, induction brown adipocytes 1 (Iba1), interleukin 6 (IL-6) expression, indicating enhanced induced proinflammatory response promoted whereas reduced inflammation shifted toward an anti-inflammatory M2 phenotype. Inhibition RAP, combined knockdown, AMPK activation shift Conclusion: modulates affecting AMPK–mTOR signaling conditions. Targeting related pathways could offer new therapeutic strategies lessen facilitate healing process after

Язык: Английский

FCGR1A Alleviates Ischemic Stroke-induced Injury by Promoting Anti-Inflammatory Microglial Polarization via the AMPK–mTOR Signaling Pathway DOI Creative Commons
Meng Liu,

Xiang‐Bing Fan,

D Chen

и другие.

Frontiers in Bioscience-Landmark, Год журнала: 2025, Номер 30(5)

Опубликована: Апрель 29, 2025

Background: Ischemic stroke triggers inflammatory responses that lead to neuronal damage, with microglial polarization significantly influencing post-stroke inflammation. This study explores the role of Fc gamma receptor Ia (FCGR1A) in and its regulatory mechanisms ischemic stroke. Methods: Differentially expressed genes (DEGs) associated were identified using GSE58294 dataset. Hub found by analyzing protein–protein interaction (PPI) networks. BV2 microglia subjected oxygen–glucose deprivation/reoxygenation (OGD/R) mimic conditions vitro, FCGR1A marker levels assessed. Besides, cells stimulated lipopolysaccharide (LPS) interferon-gamma (IFN-γ) induce M1 polarization, effects overexpression knockdown on cytokine production evaluated. The function AMP-activated protein kinase (AMPK)-mTOR pathway regulating was further investigated mTOR inhibitor rapamycin (RAP). Results: From 327 DEGs identified, chosen as a hub gene. OGD/R treatment produced time-dependent rise FCGR1A, induction brown adipocytes 1 (Iba1), interleukin 6 (IL-6) expression, indicating enhanced induced proinflammatory response promoted whereas reduced inflammation shifted toward an anti-inflammatory M2 phenotype. Inhibition RAP, combined knockdown, AMPK activation shift Conclusion: modulates affecting AMPK–mTOR signaling conditions. Targeting related pathways could offer new therapeutic strategies lessen facilitate healing process after

Язык: Английский

Процитировано

0