Expression of cellular FLICE-inhibitory protein in human coronary arteries and in a rat vascular injury model.
Expression of cellular FLICE-inhibitory protein in human coronary arteries and in a rat vascular injury model.
复制标题
细胞 FLICE 抑制蛋白在人冠状动脉和大鼠血管损伤模型中的表达。
DOI：
10.1016/s0002-9440(10)64712-8
复制
发表时间：
2000
期刊：
影响因子：
--
通讯作者：
Han,DK
中科院分区：
文献类型：
--
作者：
Imanishi,T;McBride,J;Ho,Q;O'Brien,KD;Schwartz,SM;Han,DK
We previously isolated MACH-related inducer of toxicity (MRIT), a homolog of caspase 8. MRIT, also known as c-FLICE-inhibitory protein (c-FLIP), is an enzymatically inactive homolog of caspase 8 with homology to viral FLIP (v-FLIP). Because of this homology and resemblance to dominant negative proteins, c-FLIP is widely believed to be an antagonist to the death receptor-initiated apoptotic pathways that use caspase 8. We generated a polyclonal antibody, MAG1, and show that this antibody specifically recognizes two splice forms, long form (c-FLIPl) and short form (c-FLIPs). By in situ hybridization and immunohistochemistry, we demonstrate that c-FLIP is expressed in endothelial cells, macrophages, and smooth muscle cells (SMCs) both in human coronary arteries and in cultured cells. In an uninjured rat carotid arteries, c-FLIP protein is abundant in the vascular media. After balloon angioplasty, c-FLIP protein is rapidly down-regulated in medial SMCs for 2 weeks and regains expression by 4 weeks. In contrast, the neointima is strongly immunoreactive to c-FLIP from day 7 after the initial injury and remains strongly immunoreactive until 4 to 6 weeks. Similarly there is strong c-FLIP immunoreactivity in SMCs from nonatherosclerotic diffuse intimal thickening and in the overlying endothelial cells. In contrast, c-FLIP immunoreactivity is uneven and often absent in SMCs within the atherosclerotic plaque. Double labeling with c-FLIP antibody and terminal deoxynucleotidyltransferase-mediated UDP end labeling (TUNEL) in the injured rat common carotid artery show that TUNEL-positive cells in the first 2 days after injury lack detectable c-FLIP, suggested a role for caspase 8 in this form of death. In contrast, there is no correlation of c-FLIP with the spontaneous elevation in death of intima seen at 7 days after injury. For human atherosclerotic plaques, the majority of TUNEL-positive cells lack detectable c-FLIP. The expression pattern of c-FLIP and the relation between c-FLIP and TUNEL suggest a role for c-FLIP- and caspase 8-driven death in control of viability of the cells of the atherosclerotic intima.
统计学：生物医学导论。
DOI：
--
发表时间：
1977
期刊：
影响因子：
--
作者：
M. Lavenhar;B. Brown;M. Hollander
通讯作者：
M. Hollander
动脉内溴脱氧尿苷放射增敏和放射治疗恶性星形细胞瘤。
影响因子：
4.1
作者：
Greenberg,HS;Chandler,WF;Diaz,RF;Ensminger,WD;Junck,L;Page,MA;Gebarski,SS;McKeever,P;Hood,TW;Stetson,PL
通讯作者：
Stetson,PL
用溴脱氧尿苷标记对人神经外胚层肿瘤进行原位细胞动力学研究。
影响因子：
4.1
作者：
Hoshino,T;Nagashima,T;Murovic,JA;Wilson,CB;Edwards,MS;Gutin,PH;Davis,RL;DeArmond,SJ
通讯作者：
DeArmond,SJ