Modulation of collagen XVIII/endostatin expression in lobular and biliary rat liver fibrogenesis

Jia, Jidong; Bauer, Michael; Sedlaczek, Nicolai; Herbst, Hermann; Ruehl, Martin; Hahn, Eckhart G.; Riecken, E. O.; Schuppan, Detlef

doi:10.1016/s0168-8278(01)00134-9

Cited by 27 publications

(19 citation statements)

References 29 publications

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“…Here, PVA with non-reduced flow has been observed to be associated with a significant (five-to sixfold) up-regulation. This up-regulation of procollagen I mRNA has also been observed in rat liver with biliary cirrhosis (47)(48)(49). The increase in liver hydroxyproline is paralleled by a significant up-regulation of procollagen I mRNA, which encodes the major collagen type in fibrosis.…”

Section: Discussionsupporting

confidence: 55%

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Effects of Portal Vein Arterialization on Regeneration and Morphology in Liver Transplantation: Investigations Using the Rat Model

Müller

Brummer²,

Kißler³

et al. 2004

Transplantation

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These operative techniques represent an excellent small animal model for studying the mechanism of liver regeneration and the genesis of fibrosis in liver and vessel tissue. The presenting findings indicate that the negative effects of "overarterialization" may be largely avoided by reducing portal blood flow. This implies that permanent PVA in clinical liver transplantation should be performed only in conjunction with a down-regulation of portal flow.

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Section: Discussionsupporting

confidence: 55%

“…Particularly in fibrosis of the liver, the mRNA level of procollagen I is a powerful parameter (47). Here, PVA with non-reduced flow has been observed to be associated with a significant (five-to sixfold) up-regulation.…”

Section: Discussionmentioning

confidence: 88%

Effects of Portal Vein Arterialization on Regeneration and Morphology in Liver Transplantation: Investigations Using the Rat Model

Müller

Brummer²,

Kißler³

et al. 2004

Transplantation

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“…12 Moreover, in rat models of fibrogenesis, C18 expression is upregulated in chronic biliary fibrosis, but remains constant in acute fibrogenesis. 32 However, RNA array analysis did not support the correlation between endostatin/C18 levels and cirrhosis status in HCC. 14 In the present study, immunohistochemical studies indicated that endostatin/C18 levels in tumor or nontumor tissues were not relevant to the hepatic fibrosis stages in HCC tissues (Table 1).…”

Section: Discussionmentioning

confidence: 97%

Increased endostatin/collagen XVIII expression correlates with elevated VEGF level and poor prognosis in hepatocellular carcinoma

Huang

et al. 2005

Modern Pathology

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Liver is the primary source for collagen XVIII, the precursor of angiogenesis inhibitor, endostatin. However, the role of endostatin/collagen XVIII expression during liver carcinogenesis remains elusive. Therefore, we studied its expression in five hepatoma cell lines and 105 hepatocellular carcinoma specimens. The poorly differentiated hepatoma cell lines exhibited increased endostatin/collagen XVIII levels compared with the well-differentiated ones. In hepatoma tissues, endostatin/collagen XVIII expression was detected in various types of liver cells and was significantly stronger in adjacent nontumor tissues than that in tumors (Po0.001). Endostatin/collagen XVIII expression in nontumor tissues correlated with tumor stages (P ¼ 0.014) and expression of vascular endothelial growth factor (P ¼ 0.007), but not the stages of hepatic fibrosis (P40.05). Kaplan-Meier analysis showed that patients with higher endostatin/collagen XVIII expression had significantly shorter overall survival (P ¼ 0.011) and disease-free survival (P ¼ 0.0034). Moreover, endostatin/collagen XVIII level was an independent prognostic factor for tumor recurrence (P ¼ 0.034) by multivariate analysis. In conclusion, increased endostatin/collagen XVIII expression correlated with hepatoma progression and predicted poor prognosis for patients with hepatocellular carcinoma.

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“…BEC in normal and fibrotic rat and human liver tissue (from patients with a variety of liver diseases including viral, alcoholic, and biliary) expressed mRNA for the B1 chain of laminin, the α1 chain of collagen IV, and the basement membrane proteoglycan perlecan 26, 43. BEC, along with hepatocytes, also synthesize collagen XVIII, a newly appreciated collagenous component of the basement membrane which is a precursor of the angiogenesis inhibitor endostatin 44. Synthesis of basement membrane components by BEC was observed in normal as well as fibrotic liver, with slight increases seen in fibrosis26, 41.…”

Section: Biliary Epithelial Cellsmentioning

confidence: 99%

Cellular Sources of Extracellular Matrix in Hepatic Fibrosis

Wells

2008

Clinics in Liver Disease

164

109

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Modulation of collagen XVIII/endostatin expression in lobular and biliary rat liver fibrogenesis

Cited by 27 publications

References 29 publications

Effects of Portal Vein Arterialization on Regeneration and Morphology in Liver Transplantation: Investigations Using the Rat Model

Effects of Portal Vein Arterialization on Regeneration and Morphology in Liver Transplantation: Investigations Using the Rat Model

Increased endostatin/collagen XVIII expression correlates with elevated VEGF level and poor prognosis in hepatocellular carcinoma

Cellular Sources of Extracellular Matrix in Hepatic Fibrosis

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