Expression of insulin-like growth factor-I and insulin-like growth factor binding proteins during thioacetamide-induced liver cirrhosis in rats

Novosyadlyy, Ruslan; Dargel, R.; Scharf, Jens‐Gerd

doi:10.1016/j.ghir.2005.06.015

Cited by 18 publications

(16 citation statements)

References 62 publications

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“…45 However, the primary site of TAA cytotoxicity and fibrogenesis is centrilobular. 46,47 In a recent study using rat liver precision slices, TAA was shown to induce hepatocellular cytotoxicity in a periportal location as well. 48 However, portal-tract fibrogenesis was not a prominent feature in this model, and was better induced following treatment with b-estradiol or epidermal growth factor (EGF).…”

Section: Figurementioning

confidence: 99%

Halofuginone upregulates the expression of heparanase in thioacetamide-induced liver fibrosis in rats

Ohayon

Mawasi

Pevzner

et al. 2008

Laboratory Investigation

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Section: Figurementioning

confidence: 99%

Halofuginone upregulates the expression of heparanase in thioacetamide-induced liver fibrosis in rats

Ohayon

Mawasi

Pevzner

et al. 2008

Laboratory Investigation

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“…IGFs play an important role in the regulation of metabolism, development and growth of HSC [12] . The capacity of IGFs to exert their biological effects via interactions with specific cell surface receptors is modulated by the presence of a family of structurally related IGF-binding proteins.…”

Section: Introductionmentioning

confidence: 99%

Insulin-like growth factor binding protein-7 induces activation and transdifferentiation of hepatic stellate cells in vitro

Liu¹,

Huang²,

Zhang³

et al. 2009

WJG

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AIM:To investigate the role of insulin-like growth factor binding protein-7 (IGFBP-7) in the activation and transdifferentiation of hepatic stellate cells (HSC) in vitro . METHODS:Rat HSC-T6 cells were cultured in separate dishes and treated with various concentration of transforming growth factor (TGF)-β1, IGFBP-7 or anti-IGFBP-7 antibody for 24 h. The supernatant or a cytoplasm suspension was obtained from cultured HSC, followed by transfer of cells to form cell-coated dishes. Immunocytochemistry and Western blotting were used to analyze the expression of IGFBP-7 induced by TGF-β1 and the level of fibronectin, collagen Ⅰ and α-smooth muscle actin (SMA). The pro-apoptotic effect of anti-IGFBP-7 antibody was determined by flow cytometry. RESULTS:Immunocytochemistry and Western blotting revealed that the expression of IGFBP-7 in TGF-β1 treated HSC was significantly up-regulated compared to that in the control group. In addition, fibronectin, c o l l a g e n Ⅰ a n d α-S M A a l s o s h o w e d e n h a n c e d expression in accordance with the transdifferentiation process in a dose-dependent manner to some extent. Moreover, flow cytometry suggested that anti-IGFBP-7 antibody induced apoptosis of activated HSC, which is responsible for the development of liver fibrosis, and may represent a novel pathway and target for therapeutic intervention.CONCLUSION: IGFBP-7 showed increased expression in activated HSC and played an important role in the activation and transdifferentiation process of HSC. Anti-IGFBP-7 antibody may ameliorate liver fibrogenesis.

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“…After 14 days the mice were subjected to i.p. injection of thioacetamide (TAA) (Sigma-Aldrich Inc. USA) 100 mg/kg twice per week for four weeks (Novosyadlyy, Dargel, & Scharf, 2005). Then the mice were left for further two weeks without any treatment.…”

Section: Induction Of Hccmentioning

confidence: 99%

Effect of Diet Intake Imbalance in Hepatocellular Carcinoma Progression

El-Bahrawy¹,

El-Ashmawy²,

Shamloula³

et al. 2014

IJB

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Incidence of hepatocellular carcinoma (HCC) has increased sharply in the last 10 years, with an especially high incidence in Egypt. This study was conducted to evaluate the impact of unbalanced diets on liver tumor through investigation of some biochemical mediators/pathways implicated in the pathogenesis of HCC. Male albino mice were divided into two major groups: Control group and Hepatocellular carcinoma (HCC) group; each group was further divided into four subgroups according to received diet: high fat (HF), low fat (LF), high carbohydrate (HC), and low carbohydrate (LC) groups. The results indicated that induction of HCC in mice showed marked body weight loss. Liver sections of HCC groups showed malignant giant cells and strong expression of p53. HCC mice groups kept on HF and LC diets showed the lowest survival rate, a significant increase in glucose-6-phosphate dehydrogenase (G6PDH), aldolase, and citrate synthase activities, a significant increase in serum E-cadherin as well as a significant decrease in insulin-like growth factor-1 (IGF-1) compared with LF diet. These results suggest that the molecular pathogenesis of HCC in mice correlates reduction of serum IGF-1 and elevated serum E-cadherin accompanied by reprogrammed metabolic profile shifted towards increased glycolysis and lipogenesis. These pathogenic changes were enhanced by over-consumption of carbohydrates, fats, and proteins, whereas dietary fat restriction could have a protective/ameliorative effect against the incidence of HCC.

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Expression of insulin-like growth factor-I and insulin-like growth factor binding proteins during thioacetamide-induced liver cirrhosis in rats

Cited by 18 publications

References 62 publications

Halofuginone upregulates the expression of heparanase in thioacetamide-induced liver fibrosis in rats

Halofuginone upregulates the expression of heparanase in thioacetamide-induced liver fibrosis in rats

Insulin-like growth factor binding protein-7 induces activation and transdifferentiation of hepatic stellate cells in vitro

Effect of Diet Intake Imbalance in Hepatocellular Carcinoma Progression

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