期刊
RESPIRATORY PHYSIOLOGY & NEUROBIOLOGY
卷 251, 期 -, 页码 34-40出版社
ELSEVIER
DOI: 10.1016/j.resp.2018.02.008
关键词
MicroRNA-874; Airway remodeling; Human fetal airway smooth muscle cells; Cell proliferation; Inflammation; Extracellular matrix
Pro-inflammatory cytokines-induced airway remodeling was a significant feature of asthma disease. The aim of the present study was to explore the functional significance of miR-874 in tumor necrosis factor (TNF)-alpha-treated human fetal airway smooth muscle (fASM) cells. Here, we found that TNF-alpha treatment significantly down regulated the expression of miR-874 in fASM cells. MiR-874 overexpression markedly inhibited cell viability and migration, suppressed the expression of PCNA and Ki67, reduced the expression of collagen I and collagen III, decreased the expression and activity of matrix metalloproteinase (MMP)-9 and MMP-2, and induced an obvious elevation of tissue inhibitors of metalloproteinases (TIMPs). In addition, the increased production of interleukin (IL)-6, IL-8 and eotaxin induced by TNF-alpha were significantly inhibited by miR-874 overexpression. Signal transducers and activators of transcription (STAT) 3 was identified as a direct target of miR-874, and STAT3 overexpression partly reversed the protective effects of miR-874 against TNF-alpha-induced airway remodeling. Overall, these findings demonstrate that miR-874 inhibits TNF-alpha-induced remodeling in human fASM cells at least in part by targeting STAT3.
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