首页> 外文期刊>Biochimica et biophysica acta. Molecular basis of disease: BBA >Transcripts of ceruloplasmin but not hepcidin, both major iron metabolism genes, exhibit a decreasing pattern along the portocentral axis of mouse liver
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Transcripts of ceruloplasmin but not hepcidin, both major iron metabolism genes, exhibit a decreasing pattern along the portocentral axis of mouse liver

机译:铜蓝蛋白但不是铁调素的转录物,这两个主要的铁代谢基因,均沿小鼠肝脏的中枢轴呈递减模式

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Background/aims: During iron overload of dietary origin, iron accumulates predominantly in periportal hepatocytes. A gradient in the basal and normal transcriptional control of genes involved in iron metabolism along the portocentral axis of liver lobules could explain this feature. Therefore, we aimed at characterizing, by quantitative RT-PCR, the expression of iron metabolism genes in adult C57BL/6 mouse hepatocytes regarding lobular localisation, with special emphasis to cell ploidy, considering its possible relationship with lobular zonation. Methods: We used two methods to analyse separately periportal and perivenous liver cells: 1) a selective liver zonal destruction by digitonin prior to a classical collagenase dissociation, and 2) laser capture microdissection. We also developed a method to separate viable 4N and 8N polyploid hepatocytes by flow cytometer. Results: Transcripts of ceruloplasmin, involved in iron efflux, were overexpressed in periportal areas and the result was confirmed by in situ hybridization study. By contrast, hepcidin 1, hemojuvelin, ferroportin, transferrin receptor 2, He and L-ferritin mRNAs were not differentially expressed according to either lobular zonation or polyploidisation level. Conclusions: At variance with glutamine or urea metabolism, iron metabolism is not featured by a metabolic zonation lying only on a basal transcriptional control. The preferential periportal expression of ceruloplasmin raises the issue of its special role in iron overload disorders involving a defect in cellular iron export. (C) 2008 Elsevier B.V. All rights reserved.
机译:背景/目的:在饮食中铁超负荷的过程中,铁主要积累在门静脉周围的肝细胞中。沿肝小叶的门中心轴,参与铁代谢的基因的基础和正常转录控制中的梯度可以解释此特征。因此,我们旨在通过定量RT-PCR表征成年C57BL / 6小鼠肝细胞中有关小叶定位的铁代谢基因的表达,并特别强调细胞的倍性,考虑到其可能与小叶区域的关系。方法:我们使用两种方法分别分析门静脉和静脉肝细胞:1)在经典的胶原酶解离之前,用洋地黄素选择性破坏肝区带; 2)激光捕获显微切割。我们还开发了一种通过流式细胞仪分离可行的4N和8N多倍体肝细胞的方法。结果:铜绿蛋白原的转录本参与铁外排,在门静脉周围区域过表达,该结果通过原位杂交研究得到证实。相比之下,hepcidin 1,血juvelin,ferroportin,转铁蛋白受体2,He和L-铁蛋白mRNA均未根据小叶区域或多倍体水平差异表达。结论:与谷氨酰胺或尿素代谢不同,铁代谢的特征不是仅位于基础转录控制上的代谢带。铜蓝蛋白在门口的优先表达引起了其在涉及细胞铁输出缺陷的铁超负荷疾病中的特殊作用的问题。 (C)2008 Elsevier B.V.保留所有权利。

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