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| 1 | Non-invasive biomarkers for monitoring the fibrogenic process in liver:A short survey显示文摘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. | Axel M Gressner Chun-Fang Gao Olav A Gressner | 2009 | World Journal of Gastroenterology2009，15，20： | 5 |
| 2 | Connective tissue growth factor reacts as an IL-6/STAT3-regulated hepatic negative acute phase protein显示文摘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'sera.The inhi-bition of TGFβ1 driven CCN2/CTGF expression by IL-6 did not involve a modulation of Smad2(and Smad1/3) signalling.However,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 phosphorylation.An 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. | Olav A Gressner Ieva Peredniene Axel M Gressner | 2011 | World Journal of Gastroenterology2011，17，2： | 3 |
| 3 | Variable expression of cystatin C in cultured trans-differentiating rat hepatic stellate cells显示文摘瞄准:学习 C (CysC ) ,它由转变生长 factor-beta1 (TGF-beta1 ) 的规定和导出血小板的生长因素(PDGF ) 和有在这个特殊房间发信号的 TGF-beta1 的 CysC 的潜在的干扰打的 cystatin 的表示。方法:我们计算了 CysC 表达式在有教养, profibrogenic 肝的星形细胞和区分 trans 的 myofibroblasts 由北、西方弄污并且共焦的激光扫描显微镜学。结果:CysC 在 trans 区别期间显著地被增加。TGF-beta1 和 PDGF-BB 压制了 CysC 表示。而且, CysC 分泌物被处理与 TGF-beta1 导致。尽管 CysC 导致了 TGF 贝它的一种增加的有约束力的亲密关系,受体是由化学 cross-linking 估计了与打 III (beta-glycan )[125I ] 它没调制的 -TGF-beta1, 由评估 Smad2/3 磷酸化地位出现的 TGF-beta1 信号转导变异并且[CAGA ]-MLP-luciferase 记者基因试金。有趣地,流类型 III TGF 贝它受体 beta-glycan 在对待 CysC 的房间被减少。我们的数据显示那 CysC 表情起来在 trans 区别期间调整了。结论:在患肝疾病的病人的浆液的增加的 CysC 层次是至少部分由于在激活的肝的星形细胞的更高的表情。而且, TGF-beta1 影响 CysC 的分泌物,加亮在肝的纤维发生的前进的半胱氨酸朊酶的一个潜在地重要的角色。 | Axel M Gressner Birgit Lahme Steffen K Meurer Olav Gressner Raif Weiskirchen | 2006 | World Journal of Gastroenterology2006，12，5： | 2 |
| 4 | Pro-fibrogenic potential of PDGF-D in liver fibrosis显示文摘 | Erawan Borkham-Kamphorst Claudia R.C. van Roeyen Tammo Ostendorf Jürgen Floege Axel M. Gressner Ralf Weiskirchen | 2007 | Journal of Hepatology2007，，6： | 2 |
| 5 | Roles of TGF-beta in hepatic fibrosis 显示文摘 | Gressner AM Weiskirchen R Breitkopf K | 2002 | Front Biosci2002，7，： | 1 |
| 6 | Modern pathogenetic concepts of liver fibrosis suggest stellate cells and TGF - beta as major players and therapeutic targets显示文摘 | Gressner AM Weiskirchen R | 2006 | J Cell Mol Med2006，10，1： | 1 |
| 7 | Roles of TGF-beta in hepatic fibrosis显示文摘 | Gressner AM Weiskirchen R Breitkopf K | 2002 | Front Biosci2002，7，4： | 1 |
| 8 | Connective tissue growth factor in serum as a new candidate test for assessment of hepatic fibrosis显示文摘 | Gressner AM Yagmur E Lahme B | 2006 | Clin Chem2006，52，9： | 1 |
| 9 | 显示文摘 | Gressner AM Transdifferentiation of hepatic stellate cellsdtocells)to myofibroblasts:a key event in hepatic fibrogenesis | 1996 | Kidny int1996，，： | 1 |
| 10 | Transdifferentiation of hepatic stellate cells (ho ceils) to myofibroblasts: a key event in hepatic fibrogenesis显示文摘 | Gressner AM | 1996 | Kidney Int Suppl1996，54，： | 1 |
| 11 | The cell biology of liver fibrogenesis – an imbalance of proliferation, growth arrest and apoptosis of myofibroblasts显示文摘 | Axel M. Gressner | 1998 | Cell & Tissue Research1998，，3： | 1 |
| 12 | Regulation of proteoglycan expression in fibrotic liver and cultured fat-storing cells显示文摘 | Gressner A.M N.Krull M.G.Bachem | | 0，，9： | 1 |
| 13 | Mediators of hepatic fibrogenesis显示文摘 | Gressner A M | 1996 | Hepatogastroenterology1996，43，7： | 1 |
| 14 | Cytokine and chemokine networks influencing fat-storing cells显示文摘 | Gressner AM | 2002 | J Cell Biochem Suppl2002，38，： | 1 |
| 15 | High C5a levels are associated with increased mortality in sepsis patients-No enhancing effect by actin-free Ge-globulin显示文摘 | Gressner O A Koch A Sanson E | 2008 | Clinical Biochemistry2008，41，12： | 1 |
| 16 | Cytokines and cellular crosstalk involved in the activation of fat-storing cells显示文摘 | Gressner AM | 1995 | J Hepatol1995，22，2： | 1 |
| 17 | TAp63ct induces apoptosis by activating signaling via death receptors and mitochondria 显示文摘 | Gressner O Schilling T Lorenz K | 2005 | Embo J2005，，24： | 1 |
| 18 | BMP-7 as antagonist of organ fibrosis显示文摘 | Weiskirchen R Meurer SK Gressner OA | 2009 | Front Biosci(Landmark Ed)2009，14，： | 1 |
| 19 | Differentialeffects of TGF - β on connective tissue growth factor ( CTGF /CCN2) expression in hepatic stellate cells and hepatocytes显示文摘 | GRESSNER OA LAHME B DEMIRCI I | 2007 | JHepatol2007，47，5： | 1 |
| 20 | Association of polymorphisms of the TGFβ1 gene with the rate of progression of HCV-induced liver fibrosis显示文摘 | Gewaltig J Mangasser-Stephan K Gressner AM | 2002 | Clin Chim Acta2002，316，： | 1 |
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