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首页> 外文期刊>Life sciences >Ectopic expression of MHC class II genes (RT1.B(I) beta/alpha) in rat hepatocytes in vivo and in culture can be elicited by treatment with the pregnane X receptor agonists pregnenolone 16alpha-carbonitrile and dexamethasone.
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Ectopic expression of MHC class II genes (RT1.B(I) beta/alpha) in rat hepatocytes in vivo and in culture can be elicited by treatment with the pregnane X receptor agonists pregnenolone 16alpha-carbonitrile and dexamethasone.

机译：通过用孕烷X受体激动剂孕烯醇酮16α-腈和地塞米松治疗，可以在大鼠肝细胞体内和培养中引起MHC II类基因（RT1.B（I）beta / alpha）的异位表达。

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The synthetic steroid, pregnenolone-16-alpha-carbonitrile (PCN), has served for decades as a probe for a postulated series of hepatic defenses activated under situations of environmental "stress". PCN, an antiglucocorticoid, and also such glucocorticoids as dexamethasone (Dex) appear to stimulate hepatic metabolism and elimination of xenobiotics by binding to the nuclear pregnane X receptor (PXR) which then interacts with a distinct DNA response element associated with induction of cytochrome P450 3A genes. To explore the full domain of genes controlled by PCN/PXR, we used differential display to detect rat liver mRNA species selectively induced by PCN or by Dex. Sequence analysis identified one of many PCN induced cDNA fragments as RT1.B(I)beta, a member of the major histocompatability class II (MHC) gene family usually found only in antigen presenting cells. Northern blot analysis of RNA from rat liver or from cultured hepatocytes confirmed that amounts of RT1.B(I)beta mRNA and also of its companion gene, RT1.B(I)alpha mRNA, became readily detectable within 3-6 hours following treatment with PCN or Dex, whereas no induction was observed in spleen RNA. Induction by PCN of RT1.B(I)beta immunoreactive protein was localized to the hepatocytes as judged by immunofluorescence. We conclude that ectopic expression of MHC II genes, an unprecedented effect of steroids or drugs, is rapidly evoked by PCN acting on the liver, directly. The concept of a set of genes coordinately controlled to maintain homeostasis in parenchymal tissues during toxic stress must now be extended to include the immune system.
机译：合成类固醇，孕烯醇酮-16-α-腈（PCN），已经作为环境假定“环境”下激活的一系列假定肝防御的探针，已有数十年历史。 PCN，一种抗糖皮质激素以及地塞米松（Dex）等糖皮质激素似乎通过与核孕烷X受体（PXR）结合而刺激肝脏代谢并消除异种生物，然后与与细胞色素P450 3A诱导相关的独特DNA响应元件相互作用。基因。为了探索由PCN / PXR控制的基因的完整域，我们使用差异显示来检测PCN或Dex选择性诱导的大鼠肝脏mRNA种类。序列分析将许多PCN诱导的cDNA片段之一确定为RT1.B（I）beta，这是主要在抗原呈递细胞中发现的主要组织相容性II类（MHC）基因家族的成员。大鼠肝脏或培养的肝细胞中RNA的RNA印迹分析证实，在治疗后3-6小时内可以轻易检测到RT1.B（I）beta mRNA及其伴随基因RT1.B（I）alpha mRNA的量使用PCN或Dex，但在脾RNA中未观察到诱导作用。通过PCN诱导的RT1.B（I）β免疫反应蛋白被定位在肝细胞上，通过免疫荧光判断。我们得出的结论是，PCN直接作用于肝脏会迅速引起MHC II基因的异位表达，这是类固醇或药物的空前作用。现在必须扩展一组基因控制的概念，以在毒性应激期间维持实质组织内的体内平衡，这些基因必须扩展到包括免疫系统。

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