维生素连接蛋白
细胞培养中氨基酸的稳定同位素标记
纤维化
丙型肝炎病毒
肝细胞癌
脂肪变性
病理
生物
免疫学
癌症研究
医学
蛋白质组学
细胞
病毒
纤维连接蛋白
生物化学
内分泌学
基因
作者
Claudia Montaldo,Simone Matteï,Andrea Baiocchini,Nicolina Rotiroti,Franca Del Nonno,Leopoldo Paolo Pucillo,Angela Maria Cozzolino,Cecilia Battistelli,Laura Amicone,Giuseppe Ippolito,Vera van Noort,Alice Conigliaro,Tonino Alonzi,Marco Tripodi,Carmine Mancone
出处
期刊:Proteomics
[Wiley]
日期:2014-04-14
卷期号:14 (9): 1107-1115
被引量:13
标识
DOI:10.1002/pmic.201300422
摘要
Hepatitis C virus ( HCV )‐induced iron overload has been shown to promote liver fibrosis, steatosis, and hepatocellular carcinoma. The zonal‐restricted histological distribution of pathological iron deposits has hampered the attempt to perform large‐scale in vivo molecular investigations on the comorbidity between iron and HCV . Diagnostic and prognostic markers are not yet available to assess iron overload‐induced liver fibrogenesis and progression in HCV infections. Here, by means of S pike‐in SILAC proteomic approach, we first unveiled a specific membrane protein expression signature of HCV cell cultures in the presence of iron overload. Computational analysis of proteomic dataset highlighted the hepatocytic vitronectin expression as the most promising specific biomarker for iron‐associated fibrogenesis in HCV infections. Next, the robustness of our in vitro findings was challenged in human liver biopsies by immunohistochemistry and yielded two major results: (i) hepatocytic vitronectin expression is associated to liver fibrogenesis in HCV ‐infected patients with iron overload; (ii) hepatic vitronectin expression was found to discriminate also the transition between mild to moderate fibrosis in HCV ‐infected patients without iron overload.
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