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Connective tissue growth factor reacts as an IL-6/STAT3-regulated hepatic negative acute phase protein

World Journal of Gastroenterology 2011年第2期17卷 151-163页

作者： olav A gressner Ieva Peredniene Axel M gressner Institute of Clinical Chemistry and Pathobiochemistry Central LaboratoryRWTH-University Hospital Wisplinghoff Medical Laboratories Classen-Kappelmann-Str.2450931 CologneGermany Synlab Lab Services Gubener Str.3986156 AugsburgGermany

AIM:To investigate the mechanisms involved in a possible modulator role of interleukin(IL) -6 signalling on CYR61-CTGF-NOV(CCN) 2/connective tissue growth factor(CTGF) expression in hepatocytes(PC) and to look for a relation between serum concentrations of these two parameters in patients with acute inflammation. METHODS:Expression of CCN2/CTGF,p-STAT3,p-Smad 3/1 and p-Smad2 was examined in primary freshly isolated rat or cryo-preserved human PC exposed to various stimuli by Western blotting,electrophoretic mobility shift assay(EMSA) ,reporter-gene-assays and reversetranscriptase polymerase chain reaction. RESULTS:IL-6 strongly down-regulated CCN2/CTGF protein and mRNA expression in PC,enhanceable by extracellular presence of the soluble IL-6 receptor gp80,and supported by an inverse relation between IL-6 and CCN2/CTGF concentrations in patients'*** inhi-bition of TGFβ1 driven CCN2/CTGF expression by IL-6 did not involve a modulation of Smad2(and Smad1/3) ***,the STAT3 SH2 domain binding peptide,a selective inhibitor of STAT3 DNA binding activity,counteracted the inhibitory effect of IL-6 on CCN2/CTGF expression much more pronounced than pyrrolidine-dithiocarbamate,an inhibitor primarily of STAT3 *** EMSA confirmed STAT3 binding to the proposed proximal STAT binding site in the CCN2/CTGF promoter. CONCLUSION:CCN2/CTGF is identified as a hepatocellular negative acute phase protein which is downregulated by IL-6 via the STAT3 pathway through interaction on the DNA binding level.

关键词： Hepatocytes Interleukin-6 Connective tissue growth factor STAT3 Liver fibrosis Acute phase reaction

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Non-invasive biomarkers for monitoring the fibrogenic process in liver:A short survey

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World Journal of Gastroenterology 2009年第20期15卷 2433-2440页

作者： Axel M gressner Chun-Fang Gao olav A gressner Institute of Clinical Chemistry and Pathobiochemistry Central Laboratory RWTH- University Hospital Aachen Pauwelsstr. 30 52074 Aachen Germany Department of Laboratory Medicine Eastern Hepatobiliary Hospital Second Military Medical University 225 Shanghai Road Shanghai 200438 China

The clinical course ofchronic liver diseases is significantly dependent on the progression rate and the extent offibrosis, i.e. the non-structured replacement of necrotic parenchyma by extracellular matrix. Fibrogenesis, i.e. the development offibrosis can be regarded as an unlimited wound healing process, which is based on matrix (connective tissue) synthesis in activated hepatic stellate cells, fibroblasts (fibrocytes), hepatocytes and biliary epithelial cells, which are converted to matrix-producing (myo-)fibroblasts by a process defined as epithelial-mesenchymal transition. Blood (noninvasive) biomarkers offibrogenesis and fibrosis can be divided into class and class analytes. Class biomarkers are those single tests, which are based on the pathophysiology offibrosis, whereas class biomarkers aremostly multiparametric algorithms, which have been statistically evaluated with regard to the detection and activity ofongoing fibrosis. Currently available markers fulfil the criteria ofideal clinical-chemical tests only partially, but increased understanding ofthe complex pathogenesis offibrosis offers additional ways for pathophysiologically well based serum (plasma) biomarkers. They include TGF-β-driven marker proteins, bone marrow-derived cells (fibrocytes), and cytokines, which govern proand anti-fibrotic activities. Proteomic and glycomic approaches ofserum are under investigation to set up specific protein or carbohydrate profiles in patients with liver fibrosis. These and other novel parameters will supplement or eventually replaceliver biopsy/histology, high resolution imaging analysis, and elastography for the detection and monitoring of patients at risk ofdeveloping liver fibrosis.

关键词： Biochemical markers Diagnostic validity Liver fibrosis Monitoring Multiparametric algorithms Non-invasive diagnostic tools

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Variable expression of cystatin C in cultured trans-differentiating rat hepatic stellate cells

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World Journal of Gastroenterology 2006年第5期12卷 731-738页

作者： Axel M gressner Birgit Lahme Steffen K Meurer olav gressner Raif Weiskirchen Institute of Climcal Chemistry and Pathobiochemistry RWTH Aachen UniversityD-52074 AachenGermany

AIM. To study the expression of cystatin C （CysC）, its regulation by transforming growth factor-β1 （TGF-β1） and platelet-derived growth factor （PDGF） and the potential interference of CysC with TGF-β1 signaling in this special cell type. METHODS： We evaluated the CysC expression in cultured, profibrogenic hepatic stellate cells and transdifferentiated myofibroblasts by Northern and Western blotting and confocal laser scanning microscopy. RESULTS： CysC was increased significantly in the course of trans-differentiation. Both TGF-β1 and PDGFBB suppressed CysC expression. Furthermore, CysC secretion was induced by the treatment with TGF-β1. Although CysC induced an increased binding affinity of TGF-β receptor type Ⅲ （beta-glycan） as assessed by chemical cross-linking with [^125I]-TGF-β1, it did not modulate TGF-β1 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-β receptor beta-glycan was reduced in CysC-treated cells. Our data indicated that CysC expression was upregulated during transdifferentiation. 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-β1 influences the secretion of CysC, highlighting a potentially important role of cysteine proteases in the progression of hepatic fibrogenesis.

关键词： Cystatin C TGF-β Hepatic stellate cells Tra ns-differentiation Beta-glycan

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