Expression of SPARC by activated hepatic stellate cells and its correlation with the stages of fibrogenesis in human chronic hepatitis
Expression of SPARC by activated hepatic stellate cells and its correlation with the stages of fibrogenesis in human chronic hepatitis
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DOI：
10.1007/s00428-002-0631-z
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发表时间：
2002-11-01
期刊：
影响因子：
3.5
通讯作者：
Kaneda, K
中科院分区：
文献类型：
--
作者：
Nakatani, K;Seki, S;Kaneda, K
据报道，肝硬化和肝细胞癌中的肌成纤维细胞表达富含半胱氨酸的酸性分泌蛋白 (SPARC)，其在组织重塑中发挥作用。本研究旨在揭示其在慢性肝炎中的表达。免疫光和电子显微镜表明，SPARC 由肝实质中的神经纤维和肝星状细胞 (HSC) 以及纤维间隔中的肌成纤维细胞表达。反应产物定位于粗面内质网和核膜。连续切片分析表明，HSC 共表达 SPARC、血小板衍生生长因子受体-β 和 α-平滑肌肌动蛋白。定量分析表明，虽然 SPARC 阳性 HSC 在对照肝脏中稀疏，但在慢性肝炎肝脏中，它们的数量显着增加。然而，活动等级、纤维化阶段或病因（病毒感染或自身免疫、乙型肝炎病毒或丙型肝炎病毒）之间的数量没有显着差异。然而，在肝硬化中，它们的数量显着减少。目前的结果表明，SPARC 在慢性肝炎中由活化的 HSC 表达，表明 SPARC 参与慢性损伤后的肝纤维形成。
Secreted protein, acidic and rich in cysteine (SPARC), which functions in tissue remodeling, has been reported to be expressed by myofibroblasts in liver cirrhosis and hepatocellular carcinoma. This study aimed to reveal its expression in chronic hepatitis. Immunolight and electron microscopy demonstrated that SPARC was expressed by nerve fibers and hepatic stellate cells (HSCs) in the liver parenchyma and myofibroblasts in the fibrous septa. Reaction products were localized in the rough endoplasmic reticulum and nuclear envelope. Serial section analysis demonstrated that SPARC, platelet-derived growth factor receptor-beta, and alpha-smooth muscle actin were co-expressed by HSCs. Quantitative analysis demonstrated that, while SPARC-positive HSCs were sparse in control livers, they significantly increased in number in the livers with chronic hepatitis. There were, however, no significant differences in number among the grades of activity, the stages of fibrosis, or etiology (virus-infected or autoimmune, hepatitis B virus or hepatitis C virus). In liver cirrhosis, however, they significantly decreased in number. The present results indicate that SPARC is expressed by activated HSCs in chronic hepatitis, suggesting the involvement of SPARC in hepatic fibrogenesis after chronic injuries.