第一部分:LIGHT在動脈硬化的參與角色:對巨噬細胞和血管平滑肌細胞之功能研究 第二部分:STATIN對於血管平滑肌細胞一氧化氮合成酶的基因調控探討

PART I.:Roles of LIGHT in atherosclerosis:functional assays toward macrophage and vascular smooth muscle cell PART II.: The mechanisms of statins in the regulation of inducible nitric oxide synthase gene expression on vascular smooth muscle cell

魏淳郁(Chun-yu Wei)

指導教授 ： 林琬琬

國立臺灣大學/醫學院/藥理學研究所/碩士(2004年)

https://doi.org/10.6342/NTU.2004.02116

摘要

第一部分
LIGHT是腫瘤壞死因子家族第１４個發現的成員，它的已知受體包括有LTβR，HVEM和誘餌受體DcR3。我們發現在表現有LTβR和HVEM受體的老鼠巨噬細胞及動脈血管平滑肌細胞中，LIGHT可以促使巨噬細胞潛移和吞噬oxLDL，而且LIGHT還具有使血管平滑肌細胞增生及潛移的作用。我們利用突變的LIGHT-R228E基因重組蛋白和LT

關鍵字

一氧化氮合成酶動脈硬化

並列摘要

PART I
LIGHT (homologous to lymphotoxins, shows inducible expression, and competes with herpes simplex virus glycoprotein D for herpesvirus entry mediator, a receptor expressed by T lymphocytes) is a member of the tumor necrosis factor superfamily that can interact with lymphotoxin-β receptor (LTβR), herpes virus entry mediator (HVEM), and decoy receptor (DcR3). In this study, in murine macrophages and rat aortic vascular smooth muscle cells (VSMC) expressing both LTβR and HVEM, we showed that LIGHT could induce chemotaxis and oxLDL phagocytic effect toward murine macrophage as well as proliferation and migration effects toward VSMC. Using LIGHT mutant, LIGHT-R228E, and LT

並列關鍵字

atherosclerosis ； iNOS

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