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Originally published In Press as doi:10.1074/jbc.M001763200 on April 5, 2000
J. Biol. Chem., Vol. 275, Issue 24, 18266-18270, June 16, 2000
Role of Peroxiredoxins in Regulating Intracellular Hydrogen
Peroxide and Hydrogen Peroxide-induced Apoptosis in Thyroid
Cells*
Ho
Kim,
Tae-Hoon
Lee ,
Eun Shin
Park,
Jae Mi
Suh,
Soo Jung
Park,
Hyo Kyun
Chung,
O-Yu
Kwon§,
Young Kun
Kim,
Heung Kyu
Ro, and
Minho
Shong¶
From the Departments of Internal Medicine and § Anatomy,
Chungnam National University, 640 Daesadong Chungku
Taejon 301-721, South Korea and the Korea Research
Institute of Bioscience and Biotechnology, P. O. Box 115, Yusong,
Taejon 305-600, South Korea
Peroxiredoxins (Prxs) play an important role in
regulating cellular differentiation and proliferation in several types
of mammalian cells. One mechanism for this action involves modulation of hydrogen peroxide (H2O2)-mediated
cellular responses. This report examines the expression of Prx I and
Prx II in thyroid cells and their roles in eliminating
H2O2 produced in response to thyrotropin (TSH).
Prx I and Prx II are constitutively expressed in FRTL-5 thyroid cells.
Prx I expression, but not Prx II expression, is stimulated by exposure
to TSH and H2O2. In addition, methimazole induces a high level of Prx I mRNA and protein in these cells. Overexpression of Prx I and Prx II enhances the elimination of H2O2 produced by TSH in FRTL-5 cells. Treatment
with 500 µM H2O2 causes apoptosis
in FRTL-5 cells as evidenced by standard assays of apoptosis
(i.e. terminal deoxynucleotidyl transferase deoxyuridine triphosphate-biotin nick end labeling, BAX expression, and
poly(ADP-ribose) polymerase cleavage. Overexpression of Prx I and Prx
II reduces the amount of H2O2-induced apoptosis
measured by these assays. These results suggest that Prx I and Prx II
are involved in the removal of H2O2 in thyroid
cells and can protect these cells from undergoing apoptosis. These
proteins are likely to be involved in the normal physiological response
to TSH-induced production of H2O2 in thyroid cells.
*
This work was supported by Grant HMP-98-M-2-0020 from the
Ministry of Health and Welfare and by Biotech 2000 Grant
98-N1-02-04-A-01 from the Molecular Medicine Research Group Program,
Ministry of Science and Technology, South Korea.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
¶
To whom correspondence should be addressed. Tel.:
82-42-220-7161; Fax: 82-42-257-5753; E-mail:
minhos@hanbat.chungnam.ac.kr.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.

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Copyright © 2000 by the American Society for Biochemistry and Molecular Biology.
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