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

Matsuoka S, Matsumura H, Arakawa Y, Nakamura H, Nirei K, Yamagami H, Ogawa M, Nakajima N, Amaki S, Tanaka N, Moriyama M - J Clin Biochem Nutr (2009)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Division of Gastroenterology and Hepatology, Department of Medicine, Nihon University School of Medicine, 30-1 Oyaguchi-Kamimachi, Itabashi-ku, Tokyo 173-8610, Japan.

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.

No MeSH data available.


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Localization of ICAM-1 in the livers of rats sacrificed at each time point. Intrahepatic ICAM-1 staining is diffuse and observed predominantly in the sinusoidal endothelial cells and hepatocyte membranes of the two control animals sacrificed at each time point (a and b). The intrahepatic ICAM-1 in DEN rats sacrificed at 6 weeks is expressed at moderate levels by endothelial cells and hepatocyte membranes without cellular atypia and less strongly in the membranes of hepatocytes with cellular atypia (c and d). The expression of intrahepatic ICAM-1 in DEN rats sacrificed at 8 weeks is moderate in the endothelial cells and hepatocyte membranes without cellular atypia, and slight to moderate with cellular atypia (e and f). (g) ICAM-1 expressed at higher levels in hepatocytes with strong atypia located with a map-like distribution than in areas without cellular atypia. (f) Intrahepatic ICAM-1 in the cancerous region expressed at low levels in the cancer cell membranes of rats sacrificed at 14 weeks (Counterstained by hematoxylin, original magnification: a, ×4; b, ×20; c, ×4; d, ×10; e, ×4; f, ×20; g, ×4; h, ×20).
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Figure 2: Localization of ICAM-1 in the livers of rats sacrificed at each time point. Intrahepatic ICAM-1 staining is diffuse and observed predominantly in the sinusoidal endothelial cells and hepatocyte membranes of the two control animals sacrificed at each time point (a and b). The intrahepatic ICAM-1 in DEN rats sacrificed at 6 weeks is expressed at moderate levels by endothelial cells and hepatocyte membranes without cellular atypia and less strongly in the membranes of hepatocytes with cellular atypia (c and d). The expression of intrahepatic ICAM-1 in DEN rats sacrificed at 8 weeks is moderate in the endothelial cells and hepatocyte membranes without cellular atypia, and slight to moderate with cellular atypia (e and f). (g) ICAM-1 expressed at higher levels in hepatocytes with strong atypia located with a map-like distribution than in areas without cellular atypia. (f) Intrahepatic ICAM-1 in the cancerous region expressed at low levels in the cancer cell membranes of rats sacrificed at 14 weeks (Counterstained by hematoxylin, original magnification: a, ×4; b, ×20; c, ×4; d, ×10; e, ×4; f, ×20; g, ×4; h, ×20).

Mentions: ICAM-1 expression in the liver was diffuse and observed predominantly in the sinusoidal endothelial cells and membranes of hepatocytes in the one animal of the control group sacrificed at each time point (Fig. 2a and b). ICAM-1 expression in DEN rat livers at 6 weeks was moderate in the endothelial cells and slight in the membranes of hepatocytes with atypia (Fig. 2c and d). However, the levels in both endothelial cells and hepatocyte membranes were lower than in control rats sacrificed at 6 weeks (Table 1). ICAM-1 expression in liver endothelial cells of DEN rats sacrificed at 8 weeks was slight to moderate in areas where the hepatocytes were without atypia (Fig. 2e), and only slight in areas with atypia (Fig. 2f). In particular, ICAM-1 expression was stronger in membranes of hepatocytes with strong atypia located in a map-like distribution area, than in hepatocytes without atypia (Fig. 2g). ICAM-1 expression in CA was observed in the cytoplasm and membranes of the cancer cells in rats sacrificed at 12 or 14 weeks (Fig. 2h). The expression of ICAM-1 by endothelial cells in CA was much lower than in what were considered to be normal areas of the same tissue. Moreover, ICAM-1 levels in endothelial cells tended to be lower in CA than in the AH areas and were further reduced as the density of atypical hepatocytes increased, as compared with hepatocytes in non-cancer areas. On the other hand, the expression of ICAM-1 in cell membranes and cytoplasm of cancer cells or hepatocytes with severe atypia was increased compared to hepatocytes without atypia in non-cancerous areas. In particular, the degree of expression of ICAM-1 in liver correlated with a map-like distribution or anisocytosis in irregular regeneration of hepatocytes [15–17].


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

Matsuoka S, Matsumura H, Arakawa Y, Nakamura H, Nirei K, Yamagami H, Ogawa M, Nakajima N, Amaki S, Tanaka N, Moriyama M - J Clin Biochem Nutr (2009)

Localization of ICAM-1 in the livers of rats sacrificed at each time point. Intrahepatic ICAM-1 staining is diffuse and observed predominantly in the sinusoidal endothelial cells and hepatocyte membranes of the two control animals sacrificed at each time point (a and b). The intrahepatic ICAM-1 in DEN rats sacrificed at 6 weeks is expressed at moderate levels by endothelial cells and hepatocyte membranes without cellular atypia and less strongly in the membranes of hepatocytes with cellular atypia (c and d). The expression of intrahepatic ICAM-1 in DEN rats sacrificed at 8 weeks is moderate in the endothelial cells and hepatocyte membranes without cellular atypia, and slight to moderate with cellular atypia (e and f). (g) ICAM-1 expressed at higher levels in hepatocytes with strong atypia located with a map-like distribution than in areas without cellular atypia. (f) Intrahepatic ICAM-1 in the cancerous region expressed at low levels in the cancer cell membranes of rats sacrificed at 14 weeks (Counterstained by hematoxylin, original magnification: a, ×4; b, ×20; c, ×4; d, ×10; e, ×4; f, ×20; g, ×4; h, ×20).
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Related In: Results  -  Collection

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Figure 2: Localization of ICAM-1 in the livers of rats sacrificed at each time point. Intrahepatic ICAM-1 staining is diffuse and observed predominantly in the sinusoidal endothelial cells and hepatocyte membranes of the two control animals sacrificed at each time point (a and b). The intrahepatic ICAM-1 in DEN rats sacrificed at 6 weeks is expressed at moderate levels by endothelial cells and hepatocyte membranes without cellular atypia and less strongly in the membranes of hepatocytes with cellular atypia (c and d). The expression of intrahepatic ICAM-1 in DEN rats sacrificed at 8 weeks is moderate in the endothelial cells and hepatocyte membranes without cellular atypia, and slight to moderate with cellular atypia (e and f). (g) ICAM-1 expressed at higher levels in hepatocytes with strong atypia located with a map-like distribution than in areas without cellular atypia. (f) Intrahepatic ICAM-1 in the cancerous region expressed at low levels in the cancer cell membranes of rats sacrificed at 14 weeks (Counterstained by hematoxylin, original magnification: a, ×4; b, ×20; c, ×4; d, ×10; e, ×4; f, ×20; g, ×4; h, ×20).
Mentions: ICAM-1 expression in the liver was diffuse and observed predominantly in the sinusoidal endothelial cells and membranes of hepatocytes in the one animal of the control group sacrificed at each time point (Fig. 2a and b). ICAM-1 expression in DEN rat livers at 6 weeks was moderate in the endothelial cells and slight in the membranes of hepatocytes with atypia (Fig. 2c and d). However, the levels in both endothelial cells and hepatocyte membranes were lower than in control rats sacrificed at 6 weeks (Table 1). ICAM-1 expression in liver endothelial cells of DEN rats sacrificed at 8 weeks was slight to moderate in areas where the hepatocytes were without atypia (Fig. 2e), and only slight in areas with atypia (Fig. 2f). In particular, ICAM-1 expression was stronger in membranes of hepatocytes with strong atypia located in a map-like distribution area, than in hepatocytes without atypia (Fig. 2g). ICAM-1 expression in CA was observed in the cytoplasm and membranes of the cancer cells in rats sacrificed at 12 or 14 weeks (Fig. 2h). The expression of ICAM-1 by endothelial cells in CA was much lower than in what were considered to be normal areas of the same tissue. Moreover, ICAM-1 levels in endothelial cells tended to be lower in CA than in the AH areas and were further reduced as the density of atypical hepatocytes increased, as compared with hepatocytes in non-cancer areas. On the other hand, the expression of ICAM-1 in cell membranes and cytoplasm of cancer cells or hepatocytes with severe atypia was increased compared to hepatocytes without atypia in non-cancerous areas. In particular, the degree of expression of ICAM-1 in liver correlated with a map-like distribution or anisocytosis in irregular regeneration of hepatocytes [15–17].

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Division of Gastroenterology and Hepatology, Department of Medicine, Nihon University School of Medicine, 30-1 Oyaguchi-Kamimachi, Itabashi-ku, Tokyo 173-8610, Japan.

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.

No MeSH data available.


Related in: MedlinePlus