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首页> 外文期刊>Hepatology research: the official journal of the Japan Society of Hepatology >Proinflammatory cytokines up-regulate synthesis and secretion of urinary trypsin inhibitor in human hepatoma HepG2 cells.
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Proinflammatory cytokines up-regulate synthesis and secretion of urinary trypsin inhibitor in human hepatoma HepG2 cells.

机译：促炎细胞因子上调人肝癌HepG2细胞中尿胰蛋白酶抑制剂的合成和分泌。

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Background and Aims: The urinary trypsin inhibitor (UTI), a wide range protein inhibitor synthesized by hepatocytes, is considered to play an important role not only in the protection of organ injury during severe inflammation but also in the inhibition of tumor invasion and metastasis. However, the precise mechanisms underlying control of its synthesis, secretion, and processing remain unclarified. The aim of this study is to determine whether human hepatoma HepG2 cells secrete UTI in free form and whether its synthesis and secretion are regulated by proinflammatory cytokines. Methods: Cultured HepG2 cells were stimulated using different concentrations of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta). The concentration of free UTI in the medium was measured by ELISA and the intracellular UTI precursor was identified by western blotting. UTI mRNA expression was studied by reverse transcription polymerase chain reaction (RT-PCR). Results: HepG2 cells constantly secreted free UTI and this secretion was significantly up-regulated by IL-6, IL-1beta, and TNF-alpha. IL-6, IL-1beta, and TNF-alpha enhanced the synthesis of the intracellular UTI precursor protein, and IL-1beta up-regulated UTI mRNA expression. Conclusions: HepG2 cells constantly secrete free UTI. The proinflammatory cytokines, IL-1beta, IL-6, and TNF-alpha, up-regulate UTI synthesis and secretion by up-regulating UTI mRNA expression.
机译：背景与目的：尿胰蛋白酶抑制剂（UTI）是一种由肝细胞合成的广泛蛋白抑制剂，被认为不仅在严重炎症期间保护器官损伤中起着重要作用，而且在抑制肿瘤侵袭和转移中也起着重要作用。但是，尚不清楚其合成，分泌和加工控制的确切机制。这项研究的目的是确定人类肝癌HepG2细胞是否以游离形式分泌UTI，以及其合成和分泌是否受到促炎细胞因子的调节。方法：使用不同浓度的白介素-6（IL-6），肿瘤坏死因子-α（TNF-alpha）和白介素-1β（IL-1beta）刺激培养的HepG2细胞。通过ELISA测量培养基中游离UTI的浓度，并通过western印迹鉴定细胞内UTI前体。通过逆转录聚合酶链反应（RT-PCR）研究了UTI mRNA的表达。结果：HepG2细胞不断分泌游离的UTI，并且该分泌被IL-6，IL-1beta和TNF-α显着上调。 IL-6，IL-1beta和TNF-alpha增强了细胞内UTI前体蛋白的合成，并且IL-1beta上调了UTI mRNA表达。结论：HepG2细胞不断分泌游离的UTI。促炎细胞因子IL-1beta，IL-6和TNF-alpha通过上调UTI mRNA表达来上调UTI合成和分泌。

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