HGF and Fulminant Hepatitis(Workshop1-12)
スポンサーリンク
概要
- 論文の詳細を見る
Essential histopathologic features of fulminant hepatic failure (FHF) include gradual cessation of hepatocyte proliferation, concomitant with increase in proliferation in the cellular compartment of ductular hepatocytes. These are cells with mixed hepatocyte and ductular differentiation. Studies from animal models as well as from human material have shown that these cells can differentiate into mature hepatocytes, perhaps contributing to the spontaneous recovery often observed with this syndrome. Hepatocyte Growth factor (HGF) reaches very high levels in the plasma especially during the end stage of the disease, when the above cellular changes take place. Proliferating hepatocytes in culture clonally expand as hepatoblasts under thecombined influence of HGF and EGF. Hepatoblasts revert to mature hepatocytes under the influence of basement membrane matrices. Hepatoblasts, however, become ductular hepatocytes under the influence of HGF and in the presence of collagen. Hepatocyte proliferation in culture ceases in very high concentrations of HGF. Since HGF promotes the formation of the ductular hepatocyte phenotype, and since this cellular phenotype is seen in FHF when HGF levels in the plasma are high, future therapeutic methodologies should explore the possibility that high levels of HGF during FHF are associated with hepatocyte proliferation arrest and alteration of hepatocyte differentiation to toward the ductular phenotype, thus enhancing the morbidity of FHF.
- 日本アフェレシス学会の論文