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首页> 外文期刊>Molecular and Cellular Biology >9-cis retinoic acid inhibition of activation-induced apoptosis is mediated via regulation of fas ligand and requires retinoic acid receptor and retinoid X receptor activation.
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9-cis retinoic acid inhibition of activation-induced apoptosis is mediated via regulation of fas ligand and requires retinoic acid receptor and retinoid X receptor activation.

机译：9-顺式视黄酸抑制激活诱导的凋亡是通过调节fas配体介导的，需要视黄酸受体和类维生素A X受体激活。

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T-cell hybridomas, thymocytes, and T cells can be induced to undergo apoptotic cell death by activation through the T-cell receptor. This process requires macromolecular synthesis and thus gene expression, and it has been shown to be influenced by factors regulating transcription. Recently, activation, T-cell hybridomas rapidly express the Fas/CD95 receptor and its ligand, Fas ligand (FasL), which interact to transduce the death signal in the activated cell. Retinoids, the active metabolites of vitamin A, modulate expression of specific target genes by binding to two classes of intracellular receptors, retinoic acid receptors (RARs) and retinoid X receptors (RXRs). They are potent modulators of apoptosis in a number of experimental models, and they have been shown to inhibit activation-induced apoptosis in T-cell hybridomas and thymocytes. Particularly effective is the prototypic pan-agonist 9-cis retinoic acid (9-cis RA), which has high affinity for both RARs and RXRs. We report here that 9-cis RA inhibits T-cell receptor-mediated apoptosis in T-cell hybridomas by blocking the expression of Fas ligand following activation. This inhibition appears to be at the level of FasL mRNA, with the subsequent failure to express cell surface FasL. RAR-selective (TTNPB) or RXR-selective (LG100268) ligands alone were considerably less potent than RAR-RXR pan-agonists. However, the addition of both RAR- and RXR-selective ligands was as effective as the addition of 9-cis RA alone. The demonstrates that the inhibitory effect requires the ligand-mediated activation of both retinoid receptor signaling pathways.
机译：通过T细胞受体的活化，可以诱导T细胞杂交瘤，胸腺细胞和T细胞发生凋亡性细胞死亡。该过程需要大分子合成并因此需要基因表达，并且已经显示出它受调节转录因子的影响。最近，激活的T细胞杂交瘤迅速表达Fas / CD95受体及其配体Fas配体（FasL），它们相互作用以转导激活细胞中的死亡信号。维甲酸是维生素A的活性代谢产物，它通过与两类细胞内受体，维甲酸受体（RAR）和维甲酸X受体（RXR）结合来调节特定靶基因的表达。在许多实验模型中，它们是细胞凋亡的有效调节剂，并且已显示它们抑制T细胞杂交瘤和胸腺细胞中激活诱导的细胞凋亡。原型泛激动剂9-顺式视黄酸（9-顺式RA）特别有效，它对RAR和RXR都具有很高的亲和力。我们在这里报告9顺式RA通过阻止激活后Fas配体的表达来抑制T细胞杂交瘤中T细胞受体介导的细胞凋亡。这种抑制似乎处于FasL mRNA的水平，随后未能表达细胞表面FasL。单独的RAR选择性（TTNPB）或RXR选择性（LG100268）配体的效力远低于RAR-RXR泛激动剂。但是，同时添加RAR和RXR选择性配体与单独添加9-顺式RA一样有效。证明了抑制作用需要两个类视黄醇受体信号通路的配体介导的激活。

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