当前位置:主页 > 医学论文 > 消化疾病论文 >

肝星状细胞中表皮形态发生素表达调控机制及其作用研究

发布时间:2019-01-10 08:41
【摘要】:肝星状细胞是肝脏中重要的间质细胞,是肝细胞外基质的主要来源.表皮形态发生素(epimorphin、EPM、syntaxin2)在肝脏发育、再生及癌变过程中发挥了重要的作用,目前其表达变化的调控机制及对肝星状细胞的作用还未有报道.通过对肝组织标本进行检测,发现肝纤维化过程中肝星状细胞表达EPM上调.从表观遗传学的角度对EPM表达变化调控机制进行研究,发现DNA去甲基化促进了EPM的表达.为了研究EPM对肝星状细胞的可能的调节作用,将EPM表达质粒转染肝星状细胞,之后检测了EPM对肝星状细胞增殖及迁移能力的变化.结果证明EPM能够促进肝星状细胞的增殖与迁移.本研究发现,激活的肝星状细胞高表达EPM可能是由于DNA去甲基化引起的,同时,高表达的EPM能够促进肝星状细胞的增殖与迁移,进而促进肝纤维化进展.
[Abstract]:Hepatic stellate cells are important mesenchymal cells in the liver and the main source of extracellular matrix. Epidermal morphogenetic hormone (epimorphin,EPM,syntaxin2) plays an important role in the development, regeneration and carcinogenesis of liver. The expression of EPM was up-regulated in hepatic stellate cells during hepatic fibrosis. From the perspective of epigenetics, the regulation mechanism of EPM expression change was studied. It was found that DNA demethylation promoted the expression of EPM. In order to study the possible regulatory effect of EPM on hepatic stellate cells, EPM expression plasmid was transfected into hepatic stellate cells, and then the changes of EPM on the proliferation and migration of hepatic stellate cells were detected. The results showed that EPM could promote the proliferation and migration of hepatic stellate cells. It was found that the overexpression of EPM in activated hepatic stellate cells may be due to the demethylation of DNA, and that the overexpression of EPM could promote the proliferation and migration of hepatic stellate cells and thus promote the progression of hepatic fibrosis.
【作者单位】: 解放军医学院;解放军302医院感染性疾病诊疗与研究中心;军事医学科学院野战输血研究所干细胞与再生医学研究室;
【基金】:国家自然科学基金资助项目(81200303,81470097)~~
【分类号】:R575.2

【相似文献】

相关期刊论文 前10条

1 涂传涛,张顺财;过氧化物酶体增殖物激活受体γ与肝星状细胞[J];肝脏;2002年02期

2 龚浩,张忠涛,王宇;血管紧张素Ⅱ与肝星状细胞的研究进展[J];国外医学.外科学分册;2005年06期

3 龚浩;王宇;张忠涛;李建设;马雪梅;周延忠;;血管紧张素Ⅱ及其受体拮抗剂对肝星状细胞Ⅰ型胶原合成的影响[J];首都医科大学学报;2007年01期

4 张宗h,

本文编号:2406112


资料下载
论文发表

本文链接:https://www.wllwen.com/yixuelunwen/xiaohjib/2406112.html


Copyright(c)文论论文网All Rights Reserved | 网站地图 |

版权申明:资料由用户1e50e***提供,本站仅收录摘要或目录,作者需要删除请E-mail邮箱bigeng88@qq.com