Dexamethasone-induced haptoglobin release by calf liver parenchymal cells

Hidetoshi Higuchi From the Department of Veterinary Biochemistry (Higuchi, Yuasa), and Veterinary Internal Medicine (Uchida, Takahashi), Rakuno Gakuen University, Ebetsu 069, and National Institute of Animal Health, Hokkaido Branch Laboratory (Katoh), 4 Hitsuji-gaoka, Sapporo 062, and Tohoku Branch Laboratory (Miyamoto), Shichinohe, Aomori 039-25, Japan.

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Norio Katoh From the Department of Veterinary Biochemistry (Higuchi, Yuasa), and Veterinary Internal Medicine (Uchida, Takahashi), Rakuno Gakuen University, Ebetsu 069, and National Institute of Animal Health, Hokkaido Branch Laboratory (Katoh), 4 Hitsuji-gaoka, Sapporo 062, and Tohoku Branch Laboratory (Miyamoto), Shichinohe, Aomori 039-25, Japan.

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Toru Miyamoto From the Department of Veterinary Biochemistry (Higuchi, Yuasa), and Veterinary Internal Medicine (Uchida, Takahashi), Rakuno Gakuen University, Ebetsu 069, and National Institute of Animal Health, Hokkaido Branch Laboratory (Katoh), 4 Hitsuji-gaoka, Sapporo 062, and Tohoku Branch Laboratory (Miyamoto), Shichinohe, Aomori 039-25, Japan.

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Eiji Uchida From the Department of Veterinary Biochemistry (Higuchi, Yuasa), and Veterinary Internal Medicine (Uchida, Takahashi), Rakuno Gakuen University, Ebetsu 069, and National Institute of Animal Health, Hokkaido Branch Laboratory (Katoh), 4 Hitsuji-gaoka, Sapporo 062, and Tohoku Branch Laboratory (Miyamoto), Shichinohe, Aomori 039-25, Japan.

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Akira Yuasa From the Department of Veterinary Biochemistry (Higuchi, Yuasa), and Veterinary Internal Medicine (Uchida, Takahashi), Rakuno Gakuen University, Ebetsu 069, and National Institute of Animal Health, Hokkaido Branch Laboratory (Katoh), 4 Hitsuji-gaoka, Sapporo 062, and Tohoku Branch Laboratory (Miyamoto), Shichinohe, Aomori 039-25, Japan.

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Kiyoshi Takahashi From the Department of Veterinary Biochemistry (Higuchi, Yuasa), and Veterinary Internal Medicine (Uchida, Takahashi), Rakuno Gakuen University, Ebetsu 069, and National Institute of Animal Health, Hokkaido Branch Laboratory (Katoh), 4 Hitsuji-gaoka, Sapporo 062, and Tohoku Branch Laboratory (Miyamoto), Shichinohe, Aomori 039-25, Japan.

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Summary

Parenchymal cells were isolated from the liver of male calves, and monolayer cultures formed were treated with glucocorticoids to examine whether haptoglobin, appearance of which is associated with hepatic lipidosis (fatty liver) in cattle, is induced by steroid hormones. Without addition of dexamethasone, only trace amounts of haptoglobin were detected in culture medium. With addition of dexamethasone (10−12 to 10−4 M), considerable amounts of haptoglobin were released into the medium. Maximal release was observed at concentrations of 10−8 to 10−6 M dexamethasone. Haptoglobin release was similarly induced by Cortisol, although the effect was less potent than that of dexamethasone. Actinomycin D (a known protein synthesis inhibitor) dose-dependently reduced amounts of haptoglobin released in response to 10−8 M dexamethasone. Dexamethazone also induced annexin I, which is known to be synthesized in response to glucocorticoids. Dexamethasone treatment resulted in reduced protein kinase C activity in the cell cytosol, which has been shown to be an early event in dexamethasone-treated cells. Other than glucocorticoids, estradiol induced haptoglobin release, whereas progesterone was less effective. The association of haptoglobin with hepatic lipidosis can be reasonably explained by the fact that haptoglobin production by the liver is induced by glucocorticoids and estradiol, and these steroid hormones are triggers for development of hepatic lipidosis in cattle.

Summary

Parenchymal cells were isolated from the liver of male calves, and monolayer cultures formed were treated with glucocorticoids to examine whether haptoglobin, appearance of which is associated with hepatic lipidosis (fatty liver) in cattle, is induced by steroid hormones. Without addition of dexamethasone, only trace amounts of haptoglobin were detected in culture medium. With addition of dexamethasone (10−12 to 10−4 M), considerable amounts of haptoglobin were released into the medium. Maximal release was observed at concentrations of 10−8 to 10−6 M dexamethasone. Haptoglobin release was similarly induced by Cortisol, although the effect was less potent than that of dexamethasone. Actinomycin D (a known protein synthesis inhibitor) dose-dependently reduced amounts of haptoglobin released in response to 10−8 M dexamethasone. Dexamethazone also induced annexin I, which is known to be synthesized in response to glucocorticoids. Dexamethasone treatment resulted in reduced protein kinase C activity in the cell cytosol, which has been shown to be an early event in dexamethasone-treated cells. Other than glucocorticoids, estradiol induced haptoglobin release, whereas progesterone was less effective. The association of haptoglobin with hepatic lipidosis can be reasonably explained by the fact that haptoglobin production by the liver is induced by glucocorticoids and estradiol, and these steroid hormones are triggers for development of hepatic lipidosis in cattle.

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