Regulation of luteal prostaglandin F2α production and its relevance to cell death:: An in vitro study using rat dispersed luteal cells

Regulation of luteal prostaglandin F2α production and its relevance to cell death:: An in vitro study using rat dispersed luteal cells
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DOI:
10.1016/j.prostaglandins.2006.12.003
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发表时间:
2007-06-01
影响因子:
2.9
通讯作者:
Kawaminami, Mitsumori
Kawaminami, Mitsumori
中科院分区:
生物学3区
文献类型:
--
作者:
Kurusu, Shiro;Sakaguchi, Shinya;Kawaminami, Mitsumori

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我们在体外研究了大鼠黄体细胞产生前列腺素F-2α(PGF(2α))的机制及其与细胞死亡的关系。用孕酮(P4)处理假孕第9天大鼠分散的黄体细胞,可剂量依赖性地抑制PGF(2α)的分泌。细胞因子、肿瘤坏死因子α(肿瘤坏死因子α)或干扰素γ(干扰素γ)单独没有或仅有适度的调节作用。花生四烯基三氟甲基酮(AACOCF(3))是一种特异性IVA磷脂酶A(2)抑制剂,可抑制基础和细胞因子调节的PGF(2α)的产生。联合应用肿瘤坏死因子α和干扰素-γ可刺激PGF(2α)的合成和细胞毒作用(P均<0.05)。激动型抗Fas抗体攻击可引起明显的细胞毒效应,但不影响PGF(2α)的产生。提示P4抑制大鼠黄体细胞PGF(2α)的释放,而TN-Fα和干扰素-γ协同刺激PGF(2α)的释放。他们还表明,由肿瘤坏死因子α/干扰素γ和Fas刺激引起的黄体细胞死亡似乎是通过不同的信号通路发生的,涉及PGF(2α)的产生。(C)2006 Elsevier Inc.保留所有权利。
We investigated the mechanism by which rat luteal cells produce prostaglandin F-2 alpha (PGF(2 alpha)) and its relevance to cell death in vitro. Treatment with progesterone (P4) of dispersed luteal cells prepared from rats on day 9 of pseudopregnancy caused dose-dependent inhibition of PGF(2 alpha) secretion. Cytokines, tumor necrosis factor alpha (TNF alpha) or interferon gamma (IFN gamma) alone had no or modest regulatory effects. Arachidonyl trifluoromethyl ketone (AACOCF(3)), a specific group IVA phospholipase A(2) inhibitor, depressed both basal and cytokine-regulated PGF(2 alpha) production. A combination of TNF alpha and IFN-gamma stimulated PGF(2 alpha) synthesis and cytotoxicity (both, P < 0.05). Agonistic anti-Fas antibody challenge caused a significant cytotoxic effect but without affecting PGF(2 alpha) production. The present data suggest that P4 inhibits and TN-F alpha and IFN-gamma cooperatively stimulate PGF(2 alpha) release by rat luteal cells. They also suggest that luteal cell death induced by TNF alpha/IFN gamma and Fas stimulation seems to occur via distinct signaling pathways involving PGF(2 alpha) production. (c) 2006 Elsevier Inc. All rights reserved.