Hepatocytes and the fraction of non parenchymal cells enriched with oval cells were extracted from the preneoplastic mouse liver at the stage of hyperplastic node formation and implanted into the spleen. In 14-16 months after the transplantation, multiple islets of hepatocytes which replaced up to 25% of the spleen cut area, were found in 57% (4 of 7) and 22% (8 of 36) of recipients respectively. The hepatocytes formed 2-3-cell bulks or solid masses organized into multicellular trabecules, and expressed biliary capillary antigen, albumin and transferrin. In the inoculation of nonparenchymal cell fraction, the growth of hepatic tissue in the spleen depended on the magnitude of hepatocyte admixture to be undetectable in absence of hepatocytes in the donor suspension. The growth of hepatic tissue in spleen was observed following the injection of a small number (3 x 10(-4)-6 x 10(-5)) of live hepatocytes. This fact evidences an extremely high clonogenic potency of clonogenic potency of preneoplastic hepatocytes.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Cabozantinib prevents the progression of metabolic dysfunction-associated steatohepatitis by inhibiting the activation of hepatic stellate cell and macrophage and attenuating angiogenic activity.
Heliyon
October 2024
Department of Gastroenterology, Nara Medical University, Kashihara, Nara, 634-8521, Japan.
Article Synopsis
- * In rats fed a special high-fat diet, cabozantinib treatment significantly decreased liver inflammation and fibrosis but did not change fat accumulation in liver cells, indicating its targeted impact on fibrosis rather than overall liver health.
- * The study found that cabozantinib reduced certain harmful liver cell activations and inflammatory responses without hindering liver cell regeneration, suggesting its potential for aiding liver health in cancer treatment.
A new mechanism of cancer initiation that involves the transformation of hepatocytes into preneoplastic single hepatocytes and minifoci positive for glutathione S-transferase P-form (GST-P) in rat livers: 3D analysis using a vibratome.
Cancer Med
September 2024
Department of Biomedical Sciences, Graduate School of Health Sciences, Hirosaki University, Hirosaki, Japan.
Background: Cancer initiation has long been "unknowable" in biology and medicine. In 1987, however, Moore and our research group observed single hepatocytes and minifoci that were strongly positive for glutathione S-transferase P-form (GST-P) in the rat liver as early as 2 to 3 days after initiation by diethylnitrosamine prior to the induction of GST-P foci and nodules. The induction of GST-P single hepatocytes, precursors of GST-P foci and nodules, was considered genetic.
View Article and Find Full Text PDFTumor suppressive role of the antimicrobial lectin REG3A targeting the O -GlcNAc glycosylation pathway.
Hepatology
July 2024
INSERM, U1193, Paul-Brousse University Hospital, Hepatobiliary Centre, Villejuif, France.
Background And Aims: Antimicrobial proteins of the regenerating family member 3 alpha (REG3A) family provide a first line of protection against infections and transformed cells. Their expression is inducible by inflammation, which makes their role in cancer biology less clear since an immune-inflammatory context may preexist or coexist with cancer, as occurs in HCC. The aim of this study is to clarify the role of REG3A in liver carcinogenesis and to determine whether its carbohydrate-binding functions are involved.
View Article and Find Full Text PDFHepatocyte-macrophage crosstalk via the PGRN-EGFR axis modulates ADAR1-mediated immunity in the liver.
Cell Rep
July 2024
Cancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore; NUS Center for Cancer Research, Yong Loo Lin School of Medicine, National University Singapore, Singapore, Singapore; Department of Anatomy, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore. Electronic address:
ADAR1-mediated RNA editing establishes immune tolerance to endogenous double-stranded RNA (dsRNA) by preventing its sensing, primarily by MDA5. Although deleting Ifih1 (encoding MDA5) rescues embryonic lethality in ADAR1-deficient mice, they still experience early postnatal death, and removing other MDA5 signaling proteins does not yield the same rescue. Here, we show that ablation of MDA5 in a liver-specific Adar knockout (KO) murine model fails to rescue hepatic abnormalities caused by ADAR1 loss.
View Article and Find Full Text PDFMolecular Insights of Cholestasis in MDR2 Knockout Murine Liver Organoids.
J Proteome Res
April 2024
Functional Proteomics Laboratory, Centro Nacional de Biotecnología (CSIC), Madrid 28049, Spain.
MDR3 (multidrug resistance 3) deficiency in humans (MDR2 in mice) causes progressive familial intrahepatic cholestasis type 3 (PFIC3). PFIC3 is a lethal disease characterized by an early onset of intrahepatic cholestasis progressing to liver cirrhosis, a preneoplastic condition, putting individuals at risk of hepatocellular carcinoma (HCC). Hepatocyte-like organoids from MDR2-deficient mice (MDR2KO) were used in this work to study the molecular alterations caused by the deficiency of this transporter.
View Article and Find Full Text PDFWant 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!