Retracted: miR‐145 eliminates lipopolysaccharides‐induced inflammatory injury in human fibroblast‐like synoviocyte MH7A cells

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
出处
期刊:Journal of Cellular Biochemistry [Wiley]
卷期号:119 (12): 10059-10066 被引量:9
标识
DOI:10.1002/jcb.27341
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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