The Expression of Regenerative Growth Factors in Chronic Liver Injury and Repair

Aldana, Philipp R.; Goerke, Mary E.; Carr, Sandra C.; Tracy, Thomas F.

doi:10.1006/jsre.1994.1206

Cited by 30 publications

(17 citation statements)

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“…This is associated with up-regulation of hepatocyte growth factor (HGF) and interleukin 6 (IL-6) in the peribiliary stromal and hematolymphoid cells, and these same mediators stimulate non-neoplastic BEC DNA synthesis, in vitro. [5][6][7][8][9] However, if the obstruction persists, BEC proliferation returns to near baseline levels and progressive fibrogenesis ensues. 8,10 This occurs coincidently with the induction of mitoinhibitory and fibrogenic growth factors, such as fibroblast growth factor and the TGF-␤ family of mitoinhibitory cytokines, including TGF-␤1 and activin A. Receptors for these mitogens 5 or mitoinhibitors, 11,12 respectively, are upregulated on the surface of the BEC during successive stages of the response.…”

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confidence: 99%

Growth control of human biliary epithelial cells by interleukin 6, hepatocyte growth factor, transforming growth factor β1, and activin a: Comparison of a cholangiocarcinoma cell line with primary cultures of non-neoplastic biliary epithelial cells

et al. 2000

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A well characterized human cholangiocarcinoma (CC) cell line, SG231, was compared with primary cultures of normal human biliary epithelial cells (BECs) for alterations in interleukin 6 (IL-6) and hepatocyte growth factor (HGF)-mediated stimulation and transforming growth factor ␤1 (TGF-␤1) and activin A-mediated inhibition of growth. Results were compared with immunolabeling of the original tumor and after injection of SG231 into the liver of BALB/cByJ-scid mice. In vitro, both BECs and CCs expressed met, gp80, and gp130 messenger RNA (mRNA) and protein, but the levels of expression were higher in the CCs than in the BECs. In both the CCs and BECs, exogenous HGF or IL-6 induced phosphorylation of met or gp130, respectively, and a concentration-dependent increase in DNA synthesis. However, the CCs but not BECs, continued to grow in basal serum-free medium (SFM) and spontaneously produced both IL-6 and HGF under these conditions, which resulted in auto-phosphorylation of gp130 and met, respectively; and neutralizing anti-HGF or anti-IL-6 alone inhibited CC growth, indicative of autocrine growth control circuits. Conversely, activin A inhibits the growth of both BECs and CCs, but does not significantly increase apoptosis. Activin-A-induced growth inhibition of both CCs and BECs can be reversed by 100 ng/mL exogenous IL-6, but not by 10 to 100 ng/mL HGF. TGF-␤1 inhibited the growth of BECs but had no mitoinhibitory or proapoptotic effects on CCs. Immunolabeling of the original tumor and after inoculation into scid mice showed positive staining for met, gp130, gp80, and IL-6. This study contributes to a further understanding of BEC growth control and derangements that can occur during cholangiocarcinogenesis. (HEPATOL-OGY 2000;32:26-35.)

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confidence: 99%

Growth control of human biliary epithelial cells by interleukin 6, hepatocyte growth factor, transforming growth factor β1, and activin a: Comparison of a cholangiocarcinoma cell line with primary cultures of non-neoplastic biliary epithelial cells

et al. 2000

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“…Hepatocyte injury during cholestasis is due partly to the release of proinfl ammatory mediators that cause polymorphonuclear leukocytes to accumulate in the liver and become activated to damage hepatocytes (63). Infi ltration by polymorphonuclear leukocytes may represent a source of liver injury during acute biliary obstruction in rats with bile duct ligation.…”

Section: Discussionmentioning

confidence: 99%

The protective effects of ketamine and propofol in obstructive jaundice: an experimental study

Yıldız¹,

Çoşkuner²,

Bülbüloğlu³

et al. 2012

BLL

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Abstract:Objective: In this study, we investigated the protective effects of frequently used intravenous anesthetics (ketamine, propofol, thiopental, and fentanyl) in oxidative stress in a rat liver model of obstructive jaundice. Materials and methods: Thirty-two Wistar albino rats were divided into four groups in a randomized fashion. All rats were subjected to laparotomy, common bile duct ligation and severance on day 0. Following 7 days, laparotomy was again performed using ketamine, propofol, pentobarbital, or fentanyl anesthesia. After 2 hours, the animals were sacrifi ced and tissue specimens were acquired for histopathological scoring and determination of malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) activities. Results: All rats demonstrated enlargement in the bile duct, obstructive jaundice, and histopathologic ductal proliferation. MDA and SOD levels were signifi cantly lower in the ketamine group compared with the thiopental and fentanyl groups. CAT was signifi cantly increased in the ketamine group compared with the other groups. The best portal polymorphonuclear leukocyte and necrosis scores were in the ketamine group, but this difference was not statistically signifi cant ( p=0.07) Conclusion: Ketamine and propofol were observed to cause the least amount of oxidative stress in this rat model of induced oxidative stress generated by ligation of the common bile duct. This experiment is the fi rst study on this subject in the literature (Tab. 3, Ref. 65). Full Text in PDF www.elis.sk.

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“…In fact, the increase in HGF mRNA levels in a non-ligated lobe of the liver after portal branch ligation was smaller in jaundiced rats than that in nonjaundiced rats. 45) Although liver HGF mRNA levels were elevated in biliary obstructed rats following ligation of the common bile duct, 46) the degree of increase in HGF mRNA levels may be suppressed by obstructive jaundice. Thus, liver HGF mRNA levels further increased after decompression of biliary obstruction with normalization of serum bilirubin levels.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, liver HGF mRNA levels further increased after decompression of biliary obstruction with normalization of serum bilirubin levels. 46) Although the mechanism of action of UDCA in cholestasis has not yet been elucidated, three major mechanisms of action have been suggested: protection of cholangiocytes against cytotoxicity of hydrophobic bile acids, stimulation of hepatobiliary secretion, and protection of hepatocytes against bile acid-induced apoptosis, involving inhibition of mitochondrial membrane permeability transition and possibly stimulation of a survival pathway. 47) Qiao et al 42) recently reported that UDCA caused activation of the epidermal growth factor (EGF) receptor and MAPK in rat hepatocytes in primary culture.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Hepatocyte Growth Factor Production in Human Fibroblasts by Ursodeoxycholic Acid

Hiramatsu

Matsumoto

Miyazaki

et al. 2005

Biological & Pharmaceutical Bulletin

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Hepatocyte growth factor (HGF) stimulates the proliferation of hepatocytes and biliary epithelial cells and protects hepatocytes from apoptosis induced by various stimuli. In view of HGF induction by interferons, substances used for the treatment of chronic hepatitis C, this study was conducted to determine whether ursodeoxycholic acid (UDCA), which is widely used for the treatment of cholestatic liver diseases,

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The Expression of Regenerative Growth Factors in Chronic Liver Injury and Repair

Cited by 30 publications

References 0 publications

Growth control of human biliary epithelial cells by interleukin 6, hepatocyte growth factor, transforming growth factor β1, and activin a: Comparison of a cholangiocarcinoma cell line with primary cultures of non-neoplastic biliary epithelial cells

Growth control of human biliary epithelial cells by interleukin 6, hepatocyte growth factor, transforming growth factor β1, and activin a: Comparison of a cholangiocarcinoma cell line with primary cultures of non-neoplastic biliary epithelial cells

The protective effects of ketamine and propofol in obstructive jaundice: an experimental study

Inhibition of Hepatocyte Growth Factor Production in Human Fibroblasts by Ursodeoxycholic Acid

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