PI3K/AKT/mTOR通路
细胞凋亡
下调和上调
化学
炎症
MAPK/ERK通路
蛋白激酶B
转染
成纤维细胞
细胞生物学
癌症研究
细胞培养
活力测定
脂多糖
体外
信号转导
免疫学
生物
生物化学
基因
遗传学
作者
Feng Zhong,Jian Xu,Xirui Yang,Qi Zhang,Zhaomeng Gao,Yao Deng,Lei Zhang,Chunyan Yu
摘要
Abstract Recently, it has been accepted that miR‐based therapy may be beneficial for rheumatoid arthritis (RA). This study aimed to evaluate the potential involvement of miR‐145 in RA in vitro. The expression of miR‐145 in the human fibroblast‐like synoviocyte line MH7A was overexpressed by miR‐mimic transfection, after which cells were subjected to lipopolysaccharides (LPS). Cell viability, apoptosis, and the release of pro‐inflammatory cytokines were measured. The result showed that the apoptosis and the release of IL‐1β, IL‐6, IL‐8, and TNF‐α were significantly induced by LPS. Meanwhile, LPS treatment led to downregulation of miR‐145. miR‐145 overexpression in LPS‐untreated MH7A cells had no impacts on cell apoptosis and inflammation. But, restoring miR‐145 expression in LPS‐stimulated cells by supplementation of a miR‐145 mimic protected MH7A cells against LPS‐induced apoptosis and inflammation. Furthermore, miR‐145 overexpression in LPS‐untreated MH7A cells slightly blocked the PI3K/ATK and mTOR pathways, whereas miR‐145 overexpression in LPS‐stimulated cells notably repressed the LPS‐induced activation of PI3K/ATK and MAPK/mTOR pathways. Our study suggested that miR‐145 protected MH7A cells against LPS‐induced apoptosis and inflammation by inhibiting the PI3K/AKT and MAPK/mTOR pathways.
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