Vitamin A storage in hepatic stellate cells in the regenerating rat liver: With special reference to zonal heterogeneity

Abstract

Under physiological conditions, hepatic stellate cells (HSCs) within liver lobules store about 80% of the total body vitamin A in lipid droplets in their cytoplasm, and these cells show zonal heterogeneity in terms of vitamin A-storing capacity. Vitamin A is essential for the growth and differentiation of cells, and it is well known that liver cells including HSCs show a remarkable growth capacity after partial hepatectomy (PHx). However, the status of vitamin A storage in HSCs in the liver regeneration is not yet known. Therefore, we conducted the present study to examine vitamin A storage in these cells during liver regeneration. Morphometry at the electron microscopic level, fluorescence microscopy for vitamin A autofluorescence, and immunofluorescence microscopy for desmin and ␣-smooth muscle actin (␣-SMA) were performed on sections of liver from male Wistar strain rats at various times after the animal had been subjected to 70% PHx. The mean area of vitamin A-storing lipid droplets per HSC gradually decreased toward 3 days after PHx, and then returned to normal within 14 days after it. However, the heterogeneity of vitamin A-storing lipid droplet area per HSC within the hepatic lobule disappeared after PHx and did not return to normal by 14 days thereafter, even though the liver volume had returned to normal. These results suggest that HSCs alter their vitamin A-storing capacity during liver regeneration and that the recovery of vitamin A homeostasis requires a much longer time than that for liver volume.

Aflatoxin B1 albumin adducts in plasma and aflatoxin M1 in urine are associated with plasma concentrations of vitamins A and E

“…Serum aminotransferases are the most useful measures of liver cell injury [53]. In our study, high AF-ALB was significantly associated with high ALT and high total protein and marginally associated with high AST.…”

“…Liver hepatocytes govern the uptake, transfer, metabolism, and homeostasis of vitamin A. It was previously reported [53, 71] that serum concentrations of vitamin A were lower in individuals with chronic liver diseases and were related to the severity of the condition. Hepatic stellate cells that mediate liver fibrosis are usually affected as a result of liver injury and could lead to vitamin A deficiency [72].…”

Systemic mediators induce fibrogenic effects in normal liver after partial bile duct ligation

“…Previous studies have shown that HSCs are activated 3–5 days after 70% hepatectomy (21, 22), and parameters of HSC activation are returned to control level at 14 days after operation. We did not observe increases in hepatic collagen α1(I) expression 10 days after removing the left lobectomy because the reaction of HSCs to left lobectomy might have been recovered at this time point.…”

Hepatic Stellate Cell-derived Delta-like Homolog 1 (DLK1) Protein in Liver Regeneration

“…Liver regeneration induced by partial hepatectomy (PH) is associated with the loss of HSC-associated vitamin A content (13) and up-regulation of the HSC activation markers such as ␣-smooth muscle actin (␣SMA), IL-6, and hepatocyte growth factor (14), suggesting that HSCs undergo activation and support a regenerative response. Regulation of HSC myofibroblastic activation by the neurotrophin receptor p75NTR is actually crucial for supporting liver regeneration (10).…”