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进行性家族性肝内胆汁淤积症一种亚型中多药耐药3基因表达缺陷

Defect of multidrug-resistance 3 gene expression in a subtype of progressive familial intrahepatic cholestasis.

作者信息

Deleuze J F, Jacquemin E, Dubuisson C, Cresteil D, Dumont M, Erlinger S, Bernard O, Hadchouel M

机构信息

Unité INSERM U 347, le Kremlin Bicêtre, France.

出版信息

Hepatology. 1996 Apr;23(4):904-8. doi: 10.1002/hep.510230435.

Abstract

Disruption of the murine mdr2 (multidrug-resistance) gene, which encodes a phosphatidylcholine flippase, leads to a hepatic disorder because of loss of biliary phospholipid secretion. Among the hereditary human cholestasis, a subtype of progressive familial intrahepatic cholestasis with high gamma-glutamyltranspeptidase (GGT) serum activity shares histological, biochemical, and genetic features with mice lacking mdr2 gene expression (mdr2 -/- mice). No MDR3 (human mdr2 homolog) messenger RNA (mRNA) was detected by Northern blotting in the liver of a patient suffering from this form of PFIC, and the biliary phospholipid level in a second patient was substantially decreased. Thus, the absence of the MDR3 P-glycoprotein may be responsible for this type of PFIC, which, as in the murine model, may be due to a toxic effect of bile acids on the biliary epithelium in absence of biliary phospholipids.

摘要

编码磷脂酰胆碱翻转酶的小鼠mdr2(多药耐药)基因的破坏,会因胆汁磷脂分泌缺失而导致肝脏疾病。在人类遗传性胆汁淤积症中,一种具有高γ-谷氨酰转肽酶(GGT)血清活性的进行性家族性肝内胆汁淤积症亚型,在组织学、生化和遗传学特征上与缺乏mdr2基因表达的小鼠(mdr2 -/-小鼠)相似。通过Northern印迹法在一名患有这种形式的进行性家族性肝内胆汁淤积症患者的肝脏中未检测到MDR3(人类mdr2同源物)信使核糖核酸(mRNA),并且第二名患者的胆汁磷脂水平大幅降低。因此,MDR3 P-糖蛋白的缺失可能是这种类型的进行性家族性肝内胆汁淤积症的病因,与小鼠模型一样,这可能是由于在缺乏胆汁磷脂的情况下胆汁酸对胆管上皮产生毒性作用所致。

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