Lead nitrate induces hepatocyte proliferation and subsequent apoptosis in rat livers. Iron is a constituent of heme and is also required for cell proliferation. In this study, the expression of ferritin light-chain (FTL), the major iron storage protein, was investigated in rat livers after a single intravenous injection of lead nitrate. Western blotting and immunohistochemistry revealed that FTL was increased in hepatocytes around the central veins and strongly expressed in nonparenchymal cells. Some FTL-positive nonparenchymal cells were identified as Kupffer cells that were positive for CD68. FTL-positive Kupffer cells occupied about 60% of CD68-positive cells in the periportal and perivenous areas. The relationships between FTL expression and apoptosis induction or the engulfment of apoptotic cells were examined. TUNEL-positive cells were increased in the treatment group, and enhanced expression of milk fat globule EGF-like 8 was demonstrated in some Kupffer cells and hepatocytes, indicating enhanced apoptosis induction and phagocytosis of apoptotic cells. FTL-positive Kupffer cells were not detected without lead nitrate treatment or in rat livers treated with clofibrate, which induces hepatocyte proliferation but not apoptosis. These results suggest that FTL expression in Kupffer cells after lead treatment is dependent on phagocytosis of apoptotic cells.

Download full-text PDF

Source
http://dx.doi.org/10.1177/0192623308328544DOI Listing

Publication Analysis

Top Keywords

kupffer cells
24
lead nitrate
16
cells
13
rat livers
12
apoptotic cells
12
cells lead
8
nitrate treatment
8
induces hepatocyte
8
hepatocyte proliferation
8
nonparenchymal cells
8

Similar Publications

Background/aim: Non-alcoholic fatty liver disease (NAFLD) is a global health concern with limited treatment options. The paucity of predictive   models in preclinical settings seems to be one of the limitations of identifying effective medicines. We therefore aimed to develop an   model that can display the key hallmarks of NAFLD, such as steatosis, inflammation, and fibrosis.

View Article and Find Full Text PDF

Metabolic dysfunction-associated steatotic liver disease (MASLD), previously referred to as non-alcoholic fatty liver disease, encompasses a broad range of hepatic metabolic disorders primarily characterised by the disruption of hepatic lipid metabolism, hepatic lipid accumulation and steatosis. Severe cases of MASLD might progress to metabolic dysfunction-associated steatohepatitis, characterised by hepatic inflammation, hepatocyte ballooning degeneration, activation of hepatic stellate cells (HSCs) and fibrogenesis. It may further progress to hepatocellular carcinoma.

View Article and Find Full Text PDF

Spatially restricted and ontogenically distinct hepatic macrophages are required for tissue repair.

Immunity

January 2025

Laboratory of Myeloid Cell Biology in Tissue Damage and Inflammation, VIB-UGent Center for Inflammation Research, Technologiepark-Zwijnaarde 71, Ghent 9052, Belgium; Department of Biomedical Molecular Biology, Faculty of Science, Ghent University, Ghent, Belgium. Electronic address:

Our understanding of the functional heterogeneity of resident versus recruited macrophages in the diseased liver is limited. A population of recruited lipid-associated macrophages (LAMs) has been reported to populate the diseased liver alongside resident Kupffer cells (KCs). However, the precise roles of these distinct macrophage subsets remain elusive.

View Article and Find Full Text PDF

The liver is an indispensable metabolic organ, responsible for accumulating and transporting various nutritional compounds in hepatocytes. However, the transport of these materials from the liver is an energetically intensive task because they contain a considerable number of hydrophobic components, including free cholesterol, and require specialized transfer proteins to shuttle these substances through an aqueous phase. Liver X receptors (LXRs) induce the expression of cholesterol transporters in macrophages to transport free cholesterol derived from apoptotic cells into extracellular space via high-density lipoproteins.

View Article and Find Full Text PDF

Background & Aims: Chronic hepatitis B (CHB) arises from a persistent hepatitis B virus (HBV) infection, complicating efforts for a functional cure. Kupffer cells (KCs), liver-resident macrophages, are pivotal in mediating immune tolerance to HBV. Although CD163 marks M2-polarized KCs, its precise role in HBV infection remains unclear and warrants further investigation.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!