Selenium-binding protein 1: Its physiological function, dependence on aryl hydrocarbon receptors, and role in wasting syndrome by 2,3,7,8- tetrachlorodibenzo-p-dioxin

Sayuri Tsujimoto, Takumi Ishida, Tomoki Takeda, Yuji Ishii, Yuko Onomura, Kiyomi Tsukimori, Shinji Takechi, Tadatoshi Yamaguchi, Hiroshi Uchi, Satoshi O. Suzuki, Midori Yamamoto, Masaru Himeno, Masutaka Furue, Hideyuki Yamada

研究成果: ジャーナルへの寄稿記事

11 引用 (Scopus)

抄録

Background Selenium-binding protein 1 (Selenbp1) is suggested to play a role in tumor suppression, and may be involved in the toxicity produced by dioxin, an activator of aryl hydrocarbon receptors (AhR). However, the mechanism or likelihood is largely unknown because of the limited information available about the physiological role of Selenbp1. Methods To address this issue, we generated Selenbp1-null [Selenbp1 (-/-)] mice, and examined the toxic effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in this mouse model. Results Selenbp1 (-/-) mice exhibited only a few differences from wild-type mice in their apparent phenotypes. However, a DNA microarray experiment showed that many genes including Notch1 and Cdk1, which are known to be enhanced in ovarian carcinoma, are also increased in the ovaries of Selenbp1 (-/-) mice. Based on the different responses to TCDD between C57BL/6J and DBA/2J strains of mice, the expression of Selenbp1 is suggested to be under the control of AhR. However, wasting syndrome by TCDD occurred equally in Selenbp1 (-/-) and (+/+) mice. Conclusions The above pieces of evidence suggest that 1) Selenbp1 suppresses the expression of tumor-promoting genes although a reduction in Selenbp1 alone is not very serious as far as the animals are concerned; and 2) Selenbp1 induction by TCDD is neither a pre-requisite for toxicity nor a protective response for combating TCDD toxicity. General significance Selenbp1 (-/-) mice exhibit little difference in their apparent phenotype and responsiveness to dioxin compared with the wild-type. This may be due to the compensation of Selenbp1 function by a closely-related protein, Selenbp2.

元の言語英語
ページ(範囲)3616-3624
ページ数9
ジャーナルBiochimica et Biophysica Acta - General Subjects
1830
発行部数6
DOI
出版物ステータス出版済み - 6 1 2013

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Selenium-Binding Proteins
Wasting Syndrome
Aryl Hydrocarbon Receptors
Dioxins
Toxicity
Phenotype
Tumors
Genes
Poisons
Oligonucleotide Array Sequence Analysis
Mouse Selenbp1 protein
Polychlorinated Dibenzodioxins
1,4-dioxin
Ovary
Neoplasms
Microarrays
Carcinoma
Animals

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology

これを引用

Selenium-binding protein 1 : Its physiological function, dependence on aryl hydrocarbon receptors, and role in wasting syndrome by 2,3,7,8- tetrachlorodibenzo-p-dioxin. / Tsujimoto, Sayuri; Ishida, Takumi; Takeda, Tomoki; Ishii, Yuji; Onomura, Yuko; Tsukimori, Kiyomi; Takechi, Shinji; Yamaguchi, Tadatoshi; Uchi, Hiroshi; Suzuki, Satoshi O.; Yamamoto, Midori; Himeno, Masaru; Furue, Masutaka; Yamada, Hideyuki.

:: Biochimica et Biophysica Acta - General Subjects, 巻 1830, 番号 6, 01.06.2013, p. 3616-3624.

研究成果: ジャーナルへの寄稿記事

Tsujimoto, Sayuri ; Ishida, Takumi ; Takeda, Tomoki ; Ishii, Yuji ; Onomura, Yuko ; Tsukimori, Kiyomi ; Takechi, Shinji ; Yamaguchi, Tadatoshi ; Uchi, Hiroshi ; Suzuki, Satoshi O. ; Yamamoto, Midori ; Himeno, Masaru ; Furue, Masutaka ; Yamada, Hideyuki. / Selenium-binding protein 1 : Its physiological function, dependence on aryl hydrocarbon receptors, and role in wasting syndrome by 2,3,7,8- tetrachlorodibenzo-p-dioxin. :: Biochimica et Biophysica Acta - General Subjects. 2013 ; 巻 1830, 番号 6. pp. 3616-3624.
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title = "Selenium-binding protein 1: Its physiological function, dependence on aryl hydrocarbon receptors, and role in wasting syndrome by 2,3,7,8- tetrachlorodibenzo-p-dioxin",
abstract = "Background Selenium-binding protein 1 (Selenbp1) is suggested to play a role in tumor suppression, and may be involved in the toxicity produced by dioxin, an activator of aryl hydrocarbon receptors (AhR). However, the mechanism or likelihood is largely unknown because of the limited information available about the physiological role of Selenbp1. Methods To address this issue, we generated Selenbp1-null [Selenbp1 (-/-)] mice, and examined the toxic effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in this mouse model. Results Selenbp1 (-/-) mice exhibited only a few differences from wild-type mice in their apparent phenotypes. However, a DNA microarray experiment showed that many genes including Notch1 and Cdk1, which are known to be enhanced in ovarian carcinoma, are also increased in the ovaries of Selenbp1 (-/-) mice. Based on the different responses to TCDD between C57BL/6J and DBA/2J strains of mice, the expression of Selenbp1 is suggested to be under the control of AhR. However, wasting syndrome by TCDD occurred equally in Selenbp1 (-/-) and (+/+) mice. Conclusions The above pieces of evidence suggest that 1) Selenbp1 suppresses the expression of tumor-promoting genes although a reduction in Selenbp1 alone is not very serious as far as the animals are concerned; and 2) Selenbp1 induction by TCDD is neither a pre-requisite for toxicity nor a protective response for combating TCDD toxicity. General significance Selenbp1 (-/-) mice exhibit little difference in their apparent phenotype and responsiveness to dioxin compared with the wild-type. This may be due to the compensation of Selenbp1 function by a closely-related protein, Selenbp2.",
author = "Sayuri Tsujimoto and Takumi Ishida and Tomoki Takeda and Yuji Ishii and Yuko Onomura and Kiyomi Tsukimori and Shinji Takechi and Tadatoshi Yamaguchi and Hiroshi Uchi and Suzuki, {Satoshi O.} and Midori Yamamoto and Masaru Himeno and Masutaka Furue and Hideyuki Yamada",
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AU - Tsujimoto, Sayuri

AU - Ishida, Takumi

AU - Takeda, Tomoki

AU - Ishii, Yuji

AU - Onomura, Yuko

AU - Tsukimori, Kiyomi

AU - Takechi, Shinji

AU - Yamaguchi, Tadatoshi

AU - Uchi, Hiroshi

AU - Suzuki, Satoshi O.

AU - Yamamoto, Midori

AU - Himeno, Masaru

AU - Furue, Masutaka

AU - Yamada, Hideyuki

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AB - Background Selenium-binding protein 1 (Selenbp1) is suggested to play a role in tumor suppression, and may be involved in the toxicity produced by dioxin, an activator of aryl hydrocarbon receptors (AhR). However, the mechanism or likelihood is largely unknown because of the limited information available about the physiological role of Selenbp1. Methods To address this issue, we generated Selenbp1-null [Selenbp1 (-/-)] mice, and examined the toxic effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in this mouse model. Results Selenbp1 (-/-) mice exhibited only a few differences from wild-type mice in their apparent phenotypes. However, a DNA microarray experiment showed that many genes including Notch1 and Cdk1, which are known to be enhanced in ovarian carcinoma, are also increased in the ovaries of Selenbp1 (-/-) mice. Based on the different responses to TCDD between C57BL/6J and DBA/2J strains of mice, the expression of Selenbp1 is suggested to be under the control of AhR. However, wasting syndrome by TCDD occurred equally in Selenbp1 (-/-) and (+/+) mice. Conclusions The above pieces of evidence suggest that 1) Selenbp1 suppresses the expression of tumor-promoting genes although a reduction in Selenbp1 alone is not very serious as far as the animals are concerned; and 2) Selenbp1 induction by TCDD is neither a pre-requisite for toxicity nor a protective response for combating TCDD toxicity. General significance Selenbp1 (-/-) mice exhibit little difference in their apparent phenotype and responsiveness to dioxin compared with the wild-type. This may be due to the compensation of Selenbp1 function by a closely-related protein, Selenbp2.

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