促炎细胞因子
焦点粘着
细胞生物学
氧甾醇
化学
信号转导
肿瘤坏死因子α
生物
免疫学
生物化学
炎症
胆固醇
作者
Kim Roxana Chiok Casimiro,Swechha M. Pokharel,Santanu Bose
出处
期刊:Journal of Immunology
[The American Association of Immunologists]
日期:2020-05-01
卷期号:204 (1_Supplement): 220.24-220.24
标识
DOI:10.4049/jimmunol.204.supp.220.24
摘要
Abstract We recently reported that the oxysterol 25-hydroxycholesterol (25HC), which is an oxygenated form of cholesterol, promotes proinflammatory response via Integrin-Focal Adhesion Kinase (FAK) signaling. However, it is unknown whether other non-25HC oxysterols possess similar proinflammatory activity induced by FAK signaling pathway. Thus, we tested two non-25HC oxysterols, 22-hydroxycholesterol (22HC) and 7-alphahydroxycholesterol (7-alpha-HC), for their ability to induce proinflammatory response in macrophages. Both of these oxysterols induced a proinflammatory response since we observed production of the proinflammatory cytokine tumor necrosis factor alpha (TNF) from macrophages treated with 22HC and 7-alpha-HC. Furthermore, this response was mediated via FAK signaling as TNF production from 22HC treated macrophages was abrogated in the presence of a FAK-inhibitor. Taken together, this study suggests that non-25HC oxysterols can utilize a similar signaling pathway as 25HC to induce proinflammatory response. Studies are currently in progress to dissect the molecular mechanisms involved in triggering proinflammatory response by 22HC and 7-alpha-HC.
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