期刊
TRANSPLANTATION PROCEEDINGS
卷 48, 期 8, 页码 2809-2814出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.transproceed.2016.06.043
关键词
-
资金
- National Natural Science Foundation of China [81100318]
Background. Toll-like receptor 4 (TLR4) has received a lot of attention in studies on ischemia-reperfusion (I/R) injury. TLR4 is one of the target genes for microRNA-182-5p (miR-182-5p)-mediated regulation. In this study, we evaluated the role(s) of miR-182-5p transcriptional regulation in a hepatic I/R injury model in vivo and a lipopolysaccharide (LPS)-induced inflammatory reaction model in vitro. Methods. The effects of miR-182-5p expression on the transcription and translation of TLR4 and several proinflammatory cytokines in a LPS-induced macrophage model were studied in vitro. After miR-182-5p was exogenously administered, the transcriptional/ translational profile of TLR4 and the proinfiammatory cytokines were evaluated in an in vivo I/R injury model. This data were combined with alanine transaminase expression levels and histologic features in an effort to understand the role(s) of miR-182-5p in a liver I/R model. Results. TLR4 mRNA and protein levels in LPS-induced macrophages were significantly decreased in the presence of miR-182-5p (P < .01). In vivo TLR4 mRNA and protein levels as well as the induction of several proinflammatory cytokines, including tumor necrosis factor a and interleukin-6, were decreased in the presence of miR-182-5p. Hematoxylin and eosin staining showed that edema and necrosis in I/R modes were alleviated in the miR-182-5p-expressing group compared with control. Conclusions. miR-182-5p attenuates hepatic I/R by directly suppressing TLR4.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据