Vascular adhesion molecule expression in viral chronic hepatitis: Evidence of neoangiogenesis in portal tracts

García‐Monzón, Carmelo; Sánchez-Madrid, Francisco; Garcı́a-Buey, Luisa; García-Arroyo, Alicia; Garcı́a-Sánchez, Asunción; Moreno–Otero, Ricardo

doi:10.1016/0016-5085(95)90029-2

Cited by 119 publications

(101 citation statements)

References 63 publications

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“…Recent immunohistochemical investigations point to an enhanced expression of adhesion molecules on hepatocytes, sinusoidal endothelial cells, and mononuclear inflammatory infiltrates in chronic hepatitis C, correlating with the degree of inflammation [14,[40][41][42]. In this study, expression of ICAM-1 on hepatocytes decreased in complete responders along with the improvement of inflammation.…”

Section: Discussionsupporting

confidence: 51%

Naive and memory T cell infiltrates in chronic hepatitis C: phenotypic changes with interferon treatment

Imada

Fukuda

Koyama

et al. 1997

Clinical and Experimental Immunology

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SUMMARYThe phenotypes of infiltrating lymphocytes in liver with chronic hepatitis C, including changes associated with interferon (IFN) treatment, were characterized. Specimens obtained from 22 patients treated with IFN were examined using avidin-biotin-peroxidase immunohistochemistry. In areas of lobular and periportal inflammation, most lymphocytes were CD8 þ T cells of the CD45RO þ (memory) subset. The centres of lymphoid follicles were occupied by CD20 þ B cells and a few CD4 þ T cells which were CD45RA þ (naive subset). Follicular centres were surrounded mainly with CD4 þ T cells. CD8 þ T cells, mostly CD45RO þ , were scattered through the mantle zones of follicles and extended around them. No significant changes in CD45RA þ lobular infiltrates accompanied IFN treatment. On the other hand, the number of CD45RO þ lobular infiltrates decreased after IFN treatment in complete responders (P < 0 . 01). Moreover, there were significant correlations between CD45RO þ cell counts and serum alanine aminotransferase concentrations, CD45RO þ cell counts and the liver histologic grade and CD45RO þ cell counts and CD8 þ cell counts. These results suggest that CD8 þ memory T cells participate in hepatocyte injury in chronic hepatitis C, and that a decrease of CD8 þ memory T cells correlates with the decreased liver inflammation with IFN treatment.

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Section: Discussionsupporting

confidence: 51%

Naive and memory T cell infiltrates in chronic hepatitis C: phenotypic changes with interferon treatment

Imada

Fukuda

Koyama

et al. 1997

Clinical and Experimental Immunology

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“…ulation of hypoxia-inducible factors leads to an angiogenic switch, to the upregulation of proangiogenic factors, and to the formation of neovessels 62 (Fig. 2).…”

Section: -12 Dmentioning

confidence: 99%

“…The appearance of ECs forming characteristic capillary structures in inflamed portal tracts from chronic viral hepatitis has been demonstrated. 62,74 The pathophysiological significance of chronic viral hepatitis-associated angiogenesis is presently unclear; it has been proposed to exert a beneficial role by contributing to tissue repair and regeneration after liver damage. 62 It has also been suggested to represent a risk factor for progression to hepatocellular carcinoma in patients with chronic hepatitis C. 75 The molecular mechanisms involved in chronic viral hepatitis-associated angiogenesis have not been fully identified.…”

Section: -12 Dmentioning

confidence: 99%

“…62,74 The pathophysiological significance of chronic viral hepatitis-associated angiogenesis is presently unclear; it has been proposed to exert a beneficial role by contributing to tissue repair and regeneration after liver damage. 62 It has also been suggested to represent a risk factor for progression to hepatocellular carcinoma in patients with chronic hepatitis C. 75 The molecular mechanisms involved in chronic viral hepatitis-associated angiogenesis have not been fully identified. However, many of the molecules that have been shown either in vitro or in experimental animals to participate in the angiogenic response are known to be overexpressed in the livers of such patients.…”

Section: -12 Dmentioning

confidence: 99%

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Angiogenesis in chronic inflammatory liver disease

et al. 2004

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Intrahepatic hypoxia may occur during the inflammatory and fibrotic processes that characterize several chronic liver diseases of viral and autoimmune origin. As a consequence, new vascular structures are formed to provide oxygen and nutrients. Angiogenesis involves a tightly regulated network of cellular and molecular mechanisms that result in the formation of functional vessels. Of particular importance are growth factors, molecules involved in matrix remodeling and cell migration, and vessel maturation-related factors. In recent years, a number of studies have examined the expression and function of many pro-and antiangiogenic molecules in the setting of nontumoral chronic liver diseases and liver regeneration. This review examines the potential pathogenetic role of angiogenesis in the context of viral hepatitis, cirrhosis, autoimmune hepatitis, primary biliary cirrhosis, and alcoholic liver disease. The future perspectives for research in this field are outlined.

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“…Angiogenesis is associated with hepatic inflammation [7], hepatic fibrosis [8], the formation of portosystemic collateral vessels [9], and hepatic carcinogenesis [10]. In animal models of steatohepatitis, the expression of vascular endothelial growth factor (VEGF) and angiogenesis occurred in parallel to fibrosis and carcinogenesis [11].…”

mentioning

confidence: 99%

Hepatic fibrosis developing in morbid obesity independent of steatohepatitis: new mechanism or the Rube Goldberg machine?

Kallwitz

2012

Hepatol Int

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Vascular adhesion molecule expression in viral chronic hepatitis: Evidence of neoangiogenesis in portal tracts

Cited by 119 publications

References 63 publications

Naive and memory T cell infiltrates in chronic hepatitis C: phenotypic changes with interferon treatment

Naive and memory T cell infiltrates in chronic hepatitis C: phenotypic changes with interferon treatment

Angiogenesis in chronic inflammatory liver disease

Hepatic fibrosis developing in morbid obesity independent of steatohepatitis: new mechanism or the Rube Goldberg machine?

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