Connective tissue growth factor in human liver cirrhosis

Abou-Shady, Mohamed; Frieß, Helmut; Zimmermann, Arthur; Mola, Fabio F. di; Guo, Xiaodong; Baer, H. U.; Büchler, Markus W.

doi:10.1034/j.1600-0676.2000.020004296.x

Cited by 101 publications

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“…CTGF acts as a downstream effector of TGF-b1 to stimulate fibrotic processes, promoting fibroblast proliferation, migration, and ECM production [23]. Overexpression of CTGF in liver cirrhosis, especially in fibroblasts/myofibroblasts and stellate cells, shows its important role in hepatic fibrosis [29].…”

Section: Discussionmentioning

confidence: 99%

Laser‐induced thermotherapy (LITT) elevates mRNA expression of connective tissue growth factor (CTGF) associated with reduced tumor growth of liver metastases compared to hepatic resection

et al. 2006

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Background and Objectives: Proliferation and synthesis of hepatocellular tissue after tissue damage are promoted by specific growth factors such as hepatic tissue growth factor (HGF) and connective growth factor (CTGF). Laser-induced thermotherapy (LITT) for the treatment of liver metastases is deemed to be a parenchyma-saving procedure compared to hepatic resection. The aim of this study was to compare the impact of LITT and hepatic resection on intrahepatic residual tumor tissue and expression levels of mRNA HGF/CTGF within liver and tumor tissue. Study Design/Materials and Methods: Two independent adenocarcinomas (CC531) were implanted into 75 WAG rats, one in the right (untreated tumor) and one in the left liver lobe (treated tumor). The left lobe tumor was treated either by LITT or partial hepatectomy. The control tumor was submitted to in-situ hybridization of HGF and CTGF 24-96 hours and 14 days after intervention. Results: Volumes of the untreated tumors prior to intervention were 38 AE 8 mm 3 in group I (laser), 39 AE 7 mm 3 in group II (resection), and 42 AE 12 mm 3 in group III (control) and did not differ significantly (P > 0.05). Fourteen days after the intervention the mean tumor AE SEM volume of untreated tumor in group I (laser) [223 AE 36] was smaller than in group II (resection) [1233.28 AE 181.52; P < 0.001], and in group III (control) [978.92 AE 87.57; P < 0.003]. Forty-eight hours after the intervention intrahepatic mRNA expression level of HGF in group II (resection) was almost twofold higher than in group I (laser) [7.2 AE 1.0 c/mf vs. 3.9 AE 0.4 c/mf; P < 0.01]. Fourteen days after the intervention intrahepatic mRNA expression level of CTGF in group I (laser) was higher than in group II (resection) [13.89 AE 0.77 c/mf vs. 9.09 AE 0.78 c/mf; P < 0.003]. Conclusions: LITT leads to a decrease of residual tumor growth in comparison to hepatic resection. Accelerated tumor growth after hepatic resection is associated with higher mRNA level of HGF and reduced tumor growth after LITT with higher mRNA level of CTGF. The increased CTGF-mediated regulation of ECM may cause reduced residual tumor growth after LITT.

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Section: Discussionmentioning

confidence: 99%

Laser‐induced thermotherapy (LITT) elevates mRNA expression of connective tissue growth factor (CTGF) associated with reduced tumor growth of liver metastases compared to hepatic resection

et al. 2006

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“…Accumulating evidence has suggested that upregulation of CTGF might be a central pathway during HSC activation and hepatic fibrogenesis by mediating many of the profibrotic effects of TGF-␤ (1,41,42,53). CTGF expression in HSCs is significantly enhanced during the process of activation in vitro and in vivo (41,53).…”

mentioning

confidence: 99%

Curcumin suppresses the expression of extracellular matrix genes in activated hepatic stellate cells by inhibiting gene expression of connective tissue growth factor

Zheng

Chen²

2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…[21][22][23] In addition, we and others have shown in previous works that CTGF was involved in liver fibrosis both in human chronic liver diseases and in experimental models of liver fibrosis in rats. [24][25][26] In our own study, CTGF expression was significantly associated with scores of fibrosis in chronic hepatitis, and CTGF immu-nostaining identified hepatic stellate cells (HSC) as the main source of CTGF. 24 Because NASH, a disease commonly associated with hyperglycemia and insulin resistance, is now recognized as a chronic liver disease that may lead to cirrhosis, we were interested in studying the expression of CTGF in the context of this disease both in humans and in an animal model of obesity and diabetes.…”

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confidence: 99%

High glucose and hyperinsulinemia stimulate connective tissue growth factor expression: A potential mechanism involved in progression to fibrosis in nonalcoholic steatohepatitis

et al. 2001

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Nonalcoholic steatohepatitis (NASH) may progress to liver fibrosis and cirrhosis. Mechanisms directly involved in the development of fibrosis have been poorly investigated. Because connective tissue growth factor (CTGF) is an intermediate key molecule involved in the pathogenesis of fibrosing chronic liver diseases and is potentially induced by hyperglycemia, the aims of this study were to (1) study the expression of CTGF in vivo both in human liver biopsy specimens of patients with NASH and in an experimental model of obesity and type II diabetes (Zucker rats); and (2) analyze the effects of hyperglycemia and insulin in vitro on hepatic stellate cells. In vivo, CTGF overexpression was observed in the liver tissue of all of the 16 patients with NASH. CTGF immunostaining was mild in 7 cases (44%) and moderate or strong in 9 cases (56%). Staining was mainly detected in the liver extracellular matrix in parallel with the amount of liver fibrosis. Liver from fa/fa rats also showed CTGF overexpression by comparison with Fa/fa rats both at the messenger RNA (mRNA) level (3-fold increase) and protein level. In vitro, both CTGF mRNA and protein were significantly increased when hepatic stellate cells were incubated with either glucose or insulin. A slight increase in type I procollagen mRNA level was also observed in hepatic stellate cells incubated with glucose. In conclusion, this study suggests that hyperglycemia and insulin are key-factors in the progression of fibrosis in patients with NASH through the upregulation of CTGF. (HEPATOLOGY 2001;34:738-744.)

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Connective tissue growth factor in human liver cirrhosis

Abstract: Overexpression of CTGF in liver cirrhosis, especially in fibroblasts/myofibroblasts and stellate cells, suggests that this novel factor may play an important role in hepatic fibrosis.

Cited by 101 publications

References 0 publications

Laser‐induced thermotherapy (LITT) elevates mRNA expression of connective tissue growth factor (CTGF) associated with reduced tumor growth of liver metastases compared to hepatic resection

Laser‐induced thermotherapy (LITT) elevates mRNA expression of connective tissue growth factor (CTGF) associated with reduced tumor growth of liver metastases compared to hepatic resection

Curcumin suppresses the expression of extracellular matrix genes in activated hepatic stellate cells by inhibiting gene expression of connective tissue growth factor

High glucose and hyperinsulinemia stimulate connective tissue growth factor expression: A potential mechanism involved in progression to fibrosis in nonalcoholic steatohepatitis

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