Precisely what type of cells mainly contributes to portal fibrosis, especially in chronic viral hepatitis, such as hepatic stellate cells (HSCs) in the parenchyma or myofibroblasts in the portal area, still remains unclear. It is necessary to clarify the characteristics of cells that contribute to portal fibrosis in order to determine the mechanism of portal fibrogenesis and to develop a therapeutic target for portal fibrosis. This study was undertaken to examine whether LRAT+/CRBP-1+ HSCs contribute to portal fibrosis on viral hepatitis.Antibodies to lecithin:retinol acyltransferase (LRAT), cellular retinol-binding protein-1 (CRBP-1) and widely ascertained antibodies to HSCs (alpha-smooth muscle actin, neurotrophin-3) and endothelial cells (CD31) were used for immunohistochemical studies to assess the distribution of cells that contribute to the development of portal fibrosis with the aid of fluorescence microscopy. A quantitative analysis of LRAT+/CRBP-1+ HSCs was performed.The number of LRAT+/CRBP-1+ HSCs was increased in fibrotic liver in comparison with normal liver in the portal area and fibrous septa. The number of double positive cells was less than 20% of all cells/field in maximum.This study provides evidence that functional HSCs coexpressing both LRAT and CRBP-1 that continue to maintain the ability to store vitamin A contribute in part to the development of portal fibrogenesis in addition to parenchymal fibrogenesis in patients with viral hepatitis.
A patient was a 46-year-old man. Multiple lung tumors had been pointed out on a medical examination at age 24. He came to our hospital for further examination. Multiple liver and lung tumors were found out, and epithelioid hemangioendothelioma (EHE) derived from the liver was diagnosed by biopsy. At first we gave recombinant interleukin-2 (rIL-2) by intra-arterial and local injection and then continued it by intramuscular injection for 22 years as maintenance therapy. The tumors have regressed, with partial necrosis. EHE is a rare tumor, but we do not have a standard antitumor therapy except surgical resection. This case suggests that rIL-2 may become a new therapy for EHE. We think that the report of the long-term survival of a case of EHE in which rIL-2 treatment was effective is extremely valuable.
14C-methylglucose transport in skeletal muscle was decreased by phospholipase C treatment and 14C-methyl-glucose transport in intact skeletal muscle was increased by addition of phospholipid. 14C-methy l glucose transport increased by inflammation was inhibited by anti-inflammatory drug.
