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Expression of intercellular adhesion molecule-1 in the livers of rats treated with diethylnitrosamine. | LitMetric

AI Article Synopsis

  • * Male Fisher rats were treated with diethylnitrosamine (DEN) to induce liver cancer, and ICAM-1 expression was assessed over time using various microscopy techniques.
  • * Results showed that ICAM-1 expression varied, being lower in endothelial cells but higher in hepatocyte membranes and cytoplasm as cancer developed, suggesting a potential role of ICAM-1 in the progression of chemically induced liver cancer.

Article Abstract

It has been reported that levels of soluble intercellular adhesion molecule-1 (ICAM-1) in the blood are elevated in hepatocellular carcinoma patients. In the present study, serial observations of the localization of ICAM-1 in the liver were made by light and electron microscopy in rats with carcinogen-induced cancer. Male Fisher rats were given diethylnitrosamine (DEN) orally in their drinking water. Rats were sacrificed at 6, 8, 12, or 14 weeks after the start of DEN administration and the liver tissue was collected. ICAM-1 expression in liver was assessed using indirect immunoperoxidase staining with anti-rat ICAM-1 antibody. Although ICAM-1 expression by endothelial cells in livers of DEN-treated rats was lower than in the control group at 8 weeks, it was higher in the membrane and cytoplasm of hepatocytes. The expression of ICAM-1 in mesenchymal cells was decreased, paralleling development of cellular atypia, whereas in hepatocyte membranes and cytoplasm it was increased in these atypia. ICAM-1 was localized to the cytoplasm of cancer cells, but to the membrane of hepatocytes in the treated livers at 14 weeks. Furthermore, the levels of ICAM-1 in mesenchymal cells tended to be lower in the cancerous area than in the atypical hyperplastic nodule, and were reduced as the density of cell atypia increased, in comparison to cells in areas without cancerous nodules. We concluded that ICAM-1 may be influenced the development of cancer induced in the rat liver by a chemical carcinogen.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2735624PMC
http://dx.doi.org/10.3164/jcbn.08-247DOI Listing

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