The protective role of Kupffer cells in the ischemia-reperfused rat liver
Takashi Kobayashi, Ken ichiro Hirano, Takashi Yamamoto, Go Hasegawa, Katsuyoshi Hatakeyama, Makoto Suematsu, Makoto Naito
Kupffer cells constitute a major source of the heme-degrading enzyme, heme oxygenase (HO). This study examined the roles of Kupffer cells in the modulation of accelerated heme catabolism in ischemia-reperfused rat livers. Livers from rats treated with or without liposome-encapsulated dichloromethylene diphosphonate, a Kupffer cell-depleting reagent, underwent a 20-min ligation of the portal vein followed by reperfusion, The time course of the biliary output of bilirubin, the terminal heme-degrading product, and the expression of HO-1 mRNA and protein were monitored. HO-1 mRNA levels were elevated 3 to 12 h after ischemia/reperfusion in both control and Kupffer celldepleted rats. Immunohistochemical analyses of control livers revealed that Kupffer cells expressed high levels of HO-1 while its expression in hepatocytes was low. In Kupffer cell-depleted livers, however, periportal hepatocytes displayed marked HO-1 expression. Under these conditions the two groups exhibited distinct profiles of biliary bilirubin excretion. In the controls, total bilirubin excretion increased 8-fold and peaked at 10 h after ischemia/reperfusion. In contrast, the Kupffer cell-depleting treatment resulted in a significant acceleration of the initial rise in bilirubin production, which peaked at 4 h. However, the total amount of bilirubin excreted within the initial 10 h after reperfusion was reduced by 50% as compared with that of the controls. In Kupffer cell-depleted rats, the levels of GOT and GPT as well as serum endotoxin concentrations were elevated after ischemia/reperfusion. These results suggest that Kupffer cells serve as an ischemia/reperfusion sensor that upregulates heme degradation and bilirubin excretion, and that Kupffer cells protect hepatocytes from gut-derived stressers - including endotoxin-following ischemia/reperfusion.
https://doi.org/10.1679/aohc.65.251
Published - 2002 Aug
10.1679/aohc.65.251
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Kupffer Cells Medicine & Life Sciences 100%
Ischemia Medicine & Life Sciences 62%
Bilirubin Medicine & Life Sciences 54%
Heme Oxygenase-1 Medicine & Life Sciences 43%
Kobayashi, T., Hirano, K. I., Yamamoto, T., Hasegawa, G., Hatakeyama, K., Suematsu, M., & Naito, M. (2002). The protective role of Kupffer cells in the ischemia-reperfused rat liver. Archives of Histology and Cytology, 65(3), 251-261. https://doi.org/10.1679/aohc.65.251
The protective role of Kupffer cells in the ischemia-reperfused rat liver. / Kobayashi, Takashi; Hirano, Ken ichiro; Yamamoto, Takashi et al.
In: Archives of Histology and Cytology, Vol. 65, No. 3, 08.2002, p. 251-261.
Kobayashi, T, Hirano, KI, Yamamoto, T, Hasegawa, G, Hatakeyama, K, Suematsu, M & Naito, M 2002, 'The protective role of Kupffer cells in the ischemia-reperfused rat liver', Archives of Histology and Cytology, vol. 65, no. 3, pp. 251-261. https://doi.org/10.1679/aohc.65.251
Kobayashi T, Hirano KI, Yamamoto T, Hasegawa G, Hatakeyama K, Suematsu M et al. The protective role of Kupffer cells in the ischemia-reperfused rat liver. Archives of Histology and Cytology. 2002 Aug;65(3):251-261. doi: 10.1679/aohc.65.251
Kobayashi, Takashi ; Hirano, Ken ichiro ; Yamamoto, Takashi et al. / The protective role of Kupffer cells in the ischemia-reperfused rat liver. In: Archives of Histology and Cytology. 2002 ; Vol. 65, No. 3. pp. 251-261.
@article{7d6679b3dc884390b39c0f6c49d028fb,
title = "The protective role of Kupffer cells in the ischemia-reperfused rat liver",
abstract = "Kupffer cells constitute a major source of the heme-degrading enzyme, heme oxygenase (HO). This study examined the roles of Kupffer cells in the modulation of accelerated heme catabolism in ischemia-reperfused rat livers. Livers from rats treated with or without liposome-encapsulated dichloromethylene diphosphonate, a Kupffer cell-depleting reagent, underwent a 20-min ligation of the portal vein followed by reperfusion, The time course of the biliary output of bilirubin, the terminal heme-degrading product, and the expression of HO-1 mRNA and protein were monitored. HO-1 mRNA levels were elevated 3 to 12 h after ischemia/reperfusion in both control and Kupffer celldepleted rats. Immunohistochemical analyses of control livers revealed that Kupffer cells expressed high levels of HO-1 while its expression in hepatocytes was low. In Kupffer cell-depleted livers, however, periportal hepatocytes displayed marked HO-1 expression. Under these conditions the two groups exhibited distinct profiles of biliary bilirubin excretion. In the controls, total bilirubin excretion increased 8-fold and peaked at 10 h after ischemia/reperfusion. In contrast, the Kupffer cell-depleting treatment resulted in a significant acceleration of the initial rise in bilirubin production, which peaked at 4 h. However, the total amount of bilirubin excreted within the initial 10 h after reperfusion was reduced by 50% as compared with that of the controls. In Kupffer cell-depleted rats, the levels of GOT and GPT as well as serum endotoxin concentrations were elevated after ischemia/reperfusion. These results suggest that Kupffer cells serve as an ischemia/reperfusion sensor that upregulates heme degradation and bilirubin excretion, and that Kupffer cells protect hepatocytes from gut-derived stressers - including endotoxin-following ischemia/reperfusion.",
author = "Takashi Kobayashi and Hirano, {Ken ichiro} and Takashi Yamamoto and Go Hasegawa and Katsuyoshi Hatakeyama and Makoto Suematsu and Makoto Naito",
doi = "10.1679/aohc.65.251",
journal = "Archivum Histologicum Japonicum",
publisher = "Japan Society of Histological Documentation",
T1 - The protective role of Kupffer cells in the ischemia-reperfused rat liver
AU - Kobayashi, Takashi
AU - Hirano, Ken ichiro
AU - Yamamoto, Takashi
AU - Hasegawa, Go
AU - Hatakeyama, Katsuyoshi
AU - Suematsu, Makoto
AU - Naito, Makoto
N2 - Kupffer cells constitute a major source of the heme-degrading enzyme, heme oxygenase (HO). This study examined the roles of Kupffer cells in the modulation of accelerated heme catabolism in ischemia-reperfused rat livers. Livers from rats treated with or without liposome-encapsulated dichloromethylene diphosphonate, a Kupffer cell-depleting reagent, underwent a 20-min ligation of the portal vein followed by reperfusion, The time course of the biliary output of bilirubin, the terminal heme-degrading product, and the expression of HO-1 mRNA and protein were monitored. HO-1 mRNA levels were elevated 3 to 12 h after ischemia/reperfusion in both control and Kupffer celldepleted rats. Immunohistochemical analyses of control livers revealed that Kupffer cells expressed high levels of HO-1 while its expression in hepatocytes was low. In Kupffer cell-depleted livers, however, periportal hepatocytes displayed marked HO-1 expression. Under these conditions the two groups exhibited distinct profiles of biliary bilirubin excretion. In the controls, total bilirubin excretion increased 8-fold and peaked at 10 h after ischemia/reperfusion. In contrast, the Kupffer cell-depleting treatment resulted in a significant acceleration of the initial rise in bilirubin production, which peaked at 4 h. However, the total amount of bilirubin excreted within the initial 10 h after reperfusion was reduced by 50% as compared with that of the controls. In Kupffer cell-depleted rats, the levels of GOT and GPT as well as serum endotoxin concentrations were elevated after ischemia/reperfusion. These results suggest that Kupffer cells serve as an ischemia/reperfusion sensor that upregulates heme degradation and bilirubin excretion, and that Kupffer cells protect hepatocytes from gut-derived stressers - including endotoxin-following ischemia/reperfusion.
AB - Kupffer cells constitute a major source of the heme-degrading enzyme, heme oxygenase (HO). This study examined the roles of Kupffer cells in the modulation of accelerated heme catabolism in ischemia-reperfused rat livers. Livers from rats treated with or without liposome-encapsulated dichloromethylene diphosphonate, a Kupffer cell-depleting reagent, underwent a 20-min ligation of the portal vein followed by reperfusion, The time course of the biliary output of bilirubin, the terminal heme-degrading product, and the expression of HO-1 mRNA and protein were monitored. HO-1 mRNA levels were elevated 3 to 12 h after ischemia/reperfusion in both control and Kupffer celldepleted rats. Immunohistochemical analyses of control livers revealed that Kupffer cells expressed high levels of HO-1 while its expression in hepatocytes was low. In Kupffer cell-depleted livers, however, periportal hepatocytes displayed marked HO-1 expression. Under these conditions the two groups exhibited distinct profiles of biliary bilirubin excretion. In the controls, total bilirubin excretion increased 8-fold and peaked at 10 h after ischemia/reperfusion. In contrast, the Kupffer cell-depleting treatment resulted in a significant acceleration of the initial rise in bilirubin production, which peaked at 4 h. However, the total amount of bilirubin excreted within the initial 10 h after reperfusion was reduced by 50% as compared with that of the controls. In Kupffer cell-depleted rats, the levels of GOT and GPT as well as serum endotoxin concentrations were elevated after ischemia/reperfusion. These results suggest that Kupffer cells serve as an ischemia/reperfusion sensor that upregulates heme degradation and bilirubin excretion, and that Kupffer cells protect hepatocytes from gut-derived stressers - including endotoxin-following ischemia/reperfusion.
U2 - 10.1679/aohc.65.251
DO - 10.1679/aohc.65.251
JO - Archivum Histologicum Japonicum
JF - Archivum Histologicum Japonicum