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首页> 外文期刊>The Journal of toxicological sciences >Peroxisome proliferator-activated receptor alpha agonist-induced histidine decarboxylase gene expression in the rat and mouse liver
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Peroxisome proliferator-activated receptor alpha agonist-induced histidine decarboxylase gene expression in the rat and mouse liver

机译：过氧化物酶体增殖物激活的受体α激动剂诱导的大鼠和小鼠肝脏中的组氨酸脱羧酶基因表达

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By analysis of the data from the Toxicogenomics Database (TG-GATEs), histidine decarboxylase gene (Hdc) was identified as largely and commonly upregulated by three fibratcs, clofibrate, fenofibrate, and WY-14,643, which are known to induce hepatocellular hypertrophy and proliferation via stimulation of peroxisome proliferator-activated receptor a (PPAR alpha) in rodents. As histamine has been reported to be involved in the proliferation of liver cells, the present study was conducted to focus on Hdc. Among other genes related to histidinc and histamine, the expression of the gene of histamine ammonia lyase (Hal) was exclusively mobilized by the three fibrates. The expression of Hdc, which was usually very low in the liver, was increased with the repeated administration of fibrates, and concomitantly, the constitutive expression of Hal was suppressed. An interpretation is that the formation of urocanic acid from histidine under the normal condition switches to the formation of histamine. The mobilization of gene expression of Hdc and Hal by PPAR alpha agonists could not be reproduced in primary cultured hepatocytes. The Hdc mRNA appeared to be translated to a protein which is processed differently from brain but similarly to gastric mucosa. Surprisingly, the fibrates caused hepatic hypertrophy but no induction of Hdc mRNA at all in mice. These results revealed that the changes in the histidine catabolism by PPAR alpha agonists might be partially, but not directly, involved in the hepatocyte proliferation in rats, and there is a large genetic distance even between rat and mouse.
机译：通过对毒理基因组学数据库（TG GATEs）数据的分析，组氨酸脱羧酶基因（Hdc）被三种纤维蛋白C（氯贝特、非诺贝特和WY-14643）确定为在很大程度上和通常上调，这三种纤维蛋白已知通过刺激啮齿类动物过氧化物酶体增殖物激活受体a（PPARα）诱导肝细胞肥大和增殖。由于组胺已被报道参与肝细胞的增殖，本研究的重点是Hdc。在与组氨酸和组胺相关的其他基因中，组胺解氨酶（Hal）基因的表达仅由三种贝特类激活。Hdc在肝脏中的表达通常很低，随着反复服用贝特类药物而增加，同时Hal的组成性表达受到抑制。一种解释是，在正常情况下，组氨酸生成尿氨酸转变为组胺生成。PPARα激动剂对Hdc和Hal基因表达的动员不能在原代培养的肝细胞中复制。Hdc mRNA似乎转化为一种蛋白质，其处理方式与大脑不同，但与胃粘膜类似。令人惊讶的是，贝特类药物导致小鼠肝脏肥大，但没有诱导Hdc mRNA。这些结果表明，PPARα激动剂引起的组氨酸分解代谢的变化可能部分但不是直接参与大鼠肝细胞增殖，甚至在大鼠和小鼠之间也存在很大的遗传距离。

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