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首页> 外文期刊>World Journal of Gastroenterology >Variable expression of cystatin C in cultured trans-differentiating rat hepatic stellate cells.
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Variable expression of cystatin C in cultured trans-differentiating rat hepatic stellate cells.

机译：胱抑素C在培养的转分化大鼠肝星状细胞中的可变表达。

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AIM: To study the expression of cystatin C (CysC), its regulation by transforming growth factor-beta1 (TGF-beta1) and platelet-derived growth factor (PDGF) and the potential interference of CysC with TGF-beta1 signaling in this special cell type. METHODS: We evaluated the CysC expression in cultured, profibrogenic hepatic stellate cells and trans-differentiated myofibroblasts by Northern and Western blotting and confocal laser scanning microscopy. RESULTS: CysC was increased significantly in the course of trans-differentiation. Both TGF-beta1 and PDGF-BB suppressed CysC expression. Furthermore, CysC secretion was induced by the treatment with TGF-beta1. Although CysC induced an increased binding affinity of TGF-beta receptor type III (beta-glycan) as assessed by chemical cross-linking with [125I]-TGF-beta1, it did not modulate TGF-beta1 signal transduction as shown by evaluating the Smad2/3 phosphorylation status and [CAGA]-MLP-luciferase reporter gene assay. Interestingly, the shedding of type III TGF-beta receptor beta-glycan was reduced in CysC-treated cells. Our data indicated that CysC expression was upregulated during trans-differentiation. CONCLUSION: Increased CysC levels in the serum of patients suffering from liver diseases are at least partially due to a higher expression in activated hepatic stellate cells. Furthermore, TGF-beta1 influences the secretion of CysC, highlighting a potentially important role of cysteine proteases in the progression of hepatic fibrogenesis.
机译：目的：研究半胱氨酸蛋白酶抑制剂C（CysC）的表达，其通过转化生长因子-β1（TGF-β1）和血小板源性生长因子（PDGF）的调控以及CysC对TGF-β1信号转导的潜在干扰。类型。方法：我们通过Northern和Western印迹和共聚焦激光扫描显微镜评估了培养的原纤维化肝星状细胞和转分化的成纤维细胞中CysC的表达。结果：CysC在转分化过程中显着增加。 TGF-beta1和PDGF-BB都抑制CysC表达。此外，通过用TGF-β1处理诱导了CysC分泌。尽管通过与[125I] -TGF-beta1进行化学交联评估，CysC诱导了TGF-β受体类型III（β-聚糖）的结合亲和力增加，但并未通过评估Smad2来调节TGF-β1信号转导。 / 3磷酸化状态和[CAGA] -MLP-荧光素酶报告基因测定。有趣的是，在CysC处理的细胞中，III型TGF-β受体β-聚糖的脱落减少了。我们的数据表明，CysC表达在转分化过程中被上调。结论：患有肝病的患者血清中CysC水平升高至少部分是由于活化的肝星状细胞中较高的表达。此外，TGF-beta1影响CysC的分泌，突出了半胱氨酸蛋白酶在肝纤维化进程中的潜在重要作用。

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