Neovascularization of Pericellular Fibrosis in Alcoholic Liver Disease

Abstract

The relationship between sinusoidal capillarization and pericellular fibrosis was studied in 29 specimens of human liver from patients with alcoholic liver disease. Immunohistochemically, factor VIII-related antigen was not observed in the normal sinusoidal lining cells, but was localized in the capillaries which proliferated in the pericellular fibrotic region. Fibronectin was localized in the proliferated endoplasmic reticulum of newly formed vascular endothelial cells and hepatocytes with the development of pericellular fibrosis, laminin became apparant in the plasmalemmal vesicles of capillary endothelial cells and pericytes and in the endoplasmic reticulum of mesenchymal cells in Disse's space. From these results, it was revealed that pericellular fibrosis was closely related to sinusoidal capillarization. Furthermore, it is suggested that this sinusoidal capillarization may be caused by neovascularization, and that the extracellular matrix produced by endothelial cells, hepatocytes and mesenchymal cells may promote this process. ACTA PATHOL JPN 38: 615-626, 1988.School 1-1-6, Sendagi, Bunkyo-ku, Tokyo 113, Japan. Alcoholic Liver DiseaseActa Pathol. Jpn.

Expression of LYVE-1 in sinusoidal endothelium is reduced in chronically inflamed human livers

“…LYVE-1 expression in SECs was attenuated in hepatitis/ cirrhosis in association with sinusoidal capillarization, which is generally considered to be a cirrhosis-related vascular change [7][8][9]. Hyaluronan, a ligand of LYVE-1, is mostly degraded in hepatic SECs, and is elevated in the sera of patients with advanced liver fibrosis as a consequence of SEC dysfunction related to sinusoidal capillarization [23].…”

“…Expression patterns of molecular markers are also different between SECs and common vascular endothelium [4][5][6]. In normal livers, SECs rarely express von Willebrand factor (vWf), which is generally recognized as a reliable marker of vascular endothelial cells [6][7][8][9].…”

“…Thus, cirrhotic livers lose channels for exchanging molecules between blood and hepatocytes, and their metabolic functions are severely impaired. In association with this structural change, SECs are altered to express vWf, like common vascular endothelial cells [7][8][9]. Consequently, hepatic biosynthesis of vWf and the serum levels of factor VIII are increased in patients with cirrhosis [11,12].…”

MONITORING OF MORPHOLOGICAL EFFECTS AUTOLOGICAL MESENCHIMAL STEM CELLS, TRANSPLANTED IN LIVER WITH VIRUS CYRROSIS (clinical observation)

“…Такие области часто содержали отдель-но идущие артерии и расширенные синусоиды, сви-детельствующие, по-видимому, о наличии артерио-венозных шунтов. Синусоиды, выстланные CD34-положительными эндотелиальными клетками, могут быть эквивалентны «капилляризации», как описано Шаффнером, Поппером и другими [18,22] и сохра-няться при уменьшении активности миофибробла-стов (рисунок 6а).…”

Localization of type III procollagen and prolyl 4-hydroxylase mRNAs in fibrotic human liver.

“…In a case of chronic active hepatitis, many mesenchymal cells and hepatocytes in creased in the cirrhotic human liver (13). In vitro studies have suggested that hepatocytes can produce collagens (7, 14), and play an important role in fibrogenesis and neovascularization in pathological liver (18). However, type III collagen was not detected in the cytoplasm of hepatocytes.…”