SOCS3
贾纳斯激酶
巨噬细胞极化
STAT蛋白
细胞生物学
信号转导
车站3
Janus激酶2
细胞因子
雌激素受体
生物
化学
癌症研究
免疫学
巨噬细胞
医学
内科学
生物化学
乳腺癌
体外
癌症
作者
Mingjie Shi,Zeheng Lin,Lihe Ye,Xinlin Chen,Wenfeng Zhang,Zihan Zhang,Fei Luo,Yungang Liu,Ming Shi
出处
期刊:Toxicology
[Elsevier]
日期:2020-03-01
卷期号:433-434: 152404-152404
被引量:18
标识
DOI:10.1016/j.tox.2020.152404
摘要
As an alternative to bisphenol A (BPA), bisphenol F (BPF) has been increasingly used in manufacturing various consumer products. Exposured to BPF may lead to imbalanced immune homeostasis, yet the underlying mechanisms have not been fully elucidated. The present study was aimed to investigate the effects of BPF on macrophages and the underlying mechanism in regard to its association with estrogen receptor (ER), janus kinase 2/signal transducer and activator of transcription 3/suppressor of cytokine signaling 3 (JAK2/STAT3/SOCS3) pathway. In this study, after treatment of RAW264.7 macrophages with BPF (0, 5, 10, 20 μM), the macrophage M1 polarization was promoted, and the gene expression of M1 functional markers and pro-inflammatory cytokines was upregulated, which suggested the involvement of a vicious circle associated with chronic inflammation. Moreover, BPF facilitated SOCS3 expression in the cells in a dose-dependent manner, via activation of the JAK2/STAT3 signaling pathway, which may promote the transcription of many pro-inflammatory factors. Additionally, the above effects of BPF were blocked by either JAK2/STAT3 inhibitor AG490 (10 μM) or ER antagonist ICI 182,780 (10 μM). Taken together, the results of this study indicate that BPF promotes macrophage polarization toward pro-inflammatory M1 subtype, through activation of the ER-JAK2/STAT3/SOCS3 signaling pathway. Our finding may provide a new insight into the link between bisphenol exposure and immune dysfunction.
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