Role of tumor necrosis factor or and its type I receptor in luteal regression: Induction of programmed cell death in bovine corpus luteum-derived endothelial cells
Role of tumor necrosis factor or and its type I receptor in luteal regression: Induction of programmed cell death in bovine corpus luteum-derived endothelial cells
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DOI：
10.1095/biolreprod63.6.1905
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发表时间：
2000-12-01
影响因子：
3.6
通讯作者：
Meidan, R
中科院分区：
文献类型：
--
作者：
Friedman, A;Weiss, S;Meidan, R
为探讨肿瘤坏死因子及其I型受体(TNFRI)在结构性黄体溶解中的作用，采用半定量逆转录聚合酶链式反应(RT-PCR)方法研究了TNFRI在整个发情周期黄体(CL)中的表达模式及其细胞分布。注射前列腺素F-2α的奶牛在退化的黄体组织和CL中都记录到了TNFRI mRNA水平的增加。组成Ct、类固醇生成(大小)和内皮细胞的三种主要细胞类型都表达TNFRI基因。TNFRI mRNA表达的密度分析显示，常驻内皮细胞的TNFRI mRNA水平明显高于类固醇生成的黄体细胞。在不同类型的黄体细胞中研究了与TNFRI表达相关的生理效应。肿瘤坏死因子α以剂量和时间依赖的方式诱导培养的黄体内皮细胞(LECs)程序性细胞死亡(PCD)，而不是体外黄体化类固醇激素生成细胞。有几条证据表明孕酮调节黄体细胞的存活：1)CL和LECs表达孕激素受体mRNA，2)生理水平的类固醇消除了肿瘤坏死因子α诱导的LECs的PCD，3)孕酮产生的细胞受到PCD的保护。综上所述，本研究表明，在结构性黄体溶解过程中，TNFa诱导的PCD是由TNFRI介导的，主要影响内皮细胞，而结构性黄体溶解之前孕酮的下降是启动内皮细胞凋亡的先决条件。
The role of tumor necrosis factor or (TNF alpha) and its type I receptor (TNFRI) in structural luteolysis was investigated; A semiquatitative reverse-transcription polymerase chain reaction (RT-PCR) was used to characterize the pattern of TNFRI mRNA expression within the corpus luteum (CL) throughout the estrous cycle and its cellular distribution. Increase in TNFRI mRNA levels was recorded both in regressed luteal tissue and in CL of cows injected with prostaglandin F-2 alpha. All three major cell types composing the Ct, steroidogenic (large and small) and endothelial cells expressed the TNFRI gene. A densitometric analysis of TNFRI mRNA expression revealed that resident endothelial cells had significantly higher levels of TNFRI mRNA than steroidogenic luteal cells. The physiological effects associated with TNFRI expression were investigated in the various luteal cell types. TNF alpha -induced programmed cell death (PCD) in dose- and time-dependent manners of cultured luteal endothelial cells (LECs) but not of in vitro luteinized steroidogenic cells. Several lines of evidence are provided to show that progesterone regulates luteal cell survival: 1) CL and LECs express progesterone receptor mRNA, 2) physiological levels of the steroid abolished TNF alpha -induced PCD of LECs, and 3) progesterone-producing cells are protected from PCD. In conclusion, this study suggests that TNFa-induced PCD during structural luteolysis is mediated by TNFRI, primarily affects endothelial cells, and that the decline in progesterone, preceding structural luteolysis, is a prerequisite for the initiation of apoptosis in endothelial cells.