MicroRNA-146a modulates human bronchial epithelial cell survival in response to the cytokine-induced apoptosis

被引:65
|
作者
Liu, Xiangde [1 ]
Nelson, Amy [1 ]
Wang, Xingqi [1 ]
Kanaji, Nobuhiro [1 ]
Kim, Miok [1 ]
Sato, Tadashi [1 ]
Nalanishi, Masanori [1 ]
Li, YingJi [1 ]
Sun, Jianhong [1 ]
Michalski, Joel [1 ]
Patil, Amol [1 ]
Basma, Hesham [1 ]
Rennard, Stephen I. [1 ]
机构
[1] Univ Nebraska Med Ctr, Dept Internal Med, Omaha, NE 68198 USA
关键词
miRNA; Bronchial epithelial cell; Survival; Apoptosis; CANCER-CELLS; THERAPEUTIC IMPLICATIONS; RHEUMATOID-ARTHRITIS; REDUCED EXPRESSION; SIGNALING PATHWAY; SYNOVIAL TISSUE; INFLAMMATION; LUNG; ASTHMA; INTERLEUKIN-1-BETA;
D O I
10.1016/j.bbrc.2009.01.066
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
MicroRNA plays an important role in cell differentiation, proliferation and cell death. The current study found that miRNA-146a was up-regulated in human bronchial epithelial cells (HBECs) in response to stimulation by TGF-beta 1 Plus cytomix (a mixture of IL-1 beta, IFN-gamma and TNF-alpha). TGF-beta 1 plus cytomix (TCM) induced apoptosis in HBECs (3.4 +/- 0.6% of control vs 83.1 +/- 4.0% of TCM treated cells, p < 0.01), and this was significantly blocked by the miRNA-146a mimic (8.8 +/- 1.5%, p < 0.01). In contrast, a miRNA-146a, inhibitor had only a modest effect on cell survival but appeared to augment the induction of epithelial-mesenchymal transition (EMT) in response to the cytokines. The MicroRNA-146a mimic appears to modulate HBEC survival through a mechanism of up-regulating Bcl-XL and STAT3 phosphorylation, and by this mechanism it could contribute to tissue repair and remodeling. (C) 2009 Elsevier Inc. All rights reserved
引用
收藏
页码:177 / 182
页数:6
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