Cooperation of Liver Cells in Health and Disease

ISBN-13: 9783540418870 / Angielski / Miękka / 2001 / 151 str.

Z. Kmiec; Zbigniew Kmiec

Opis

This monograph is a presentation of the emerging field of liver biology. It summarizes multiple data that suggest the important role of cellular cross-talk for the functions of both normal and diseased liver. It also includes concise presentation of the majority of detailed data in 19 tables.

Spis treści

Cells of the liver lobule.- Hepatocytes.- Sinusoidale endothelial cells.- Kupffer cells.- Hepatic stellate cells.- Pit cells and other intrahepatic lymphocytes.- Cross-talk of liver cells in physiology and pathology.- Cooperation of liver cells in eicosanoid synthesis and degradation.- Nitric oxide as a mediator of intercellular communication in the liver.- Cooperation of hepatocytes and stellate cells in the metabolisms and storage of retinoids.- Cooperation of liver cells in the regulation of glucose metabolism.- Cooperation of liver cells in the synthesis of growth factors and growth factor binding proteins.- Cooperation of liver cells in the regulation of sinusoidal contractility.- Cross-talk of liver cells in response to endotoxin.- Endotoxin uptake by the liver.- Cooperation of liver cells in the process of liver fibrosis.- Perspectives.- Summary.- References.- Subject Index.

Blurb

The book is the first monograph that describes the importance of the interactions between hepatocytes and nonparenchymal liver cells for the functions of both normal and diseased liver. The concise description of major types of non-hepatocytes (sinusoidal endothelial cells, Kupffer cells, hepatic stellate cells, pit cells and other intrahepatic lymphocytes) has been followed by the presentation of the role of cellular cross-talks for the physiological regulation of specific liver functions such as uptake and storage of vitamin A, modulation of glucose homeostasis, sinusoidal blood flow regulation, synthesis of eicosanoids, nitric oxide, and growth factors. The functioning of complicated intercellular networks during the course of endotoxin-induced liver damage, and development of liver fibrosis has also been presented.