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Title 

Role of peroxiredoxins in regulating intracellular hydrogen peroxide and hydrogen peroxide-induced apoptosis in thyroid cells

Authors 

Ho KimTae Hoon LeeEun Shin ParkJae Mi SuhSoo Jung ParkHyo Kyun ChungO Yu KwonYoung Kun KimHeung Kyu RoMin Ho Shong

Publisher 

American Society for Biochemistry and Molecular Biology

Issue Date 

2000

Citation 

Journal of Biological Chemistry, vol. 275, no. 24, pp. 18266-18270

Keywords 

hydrogen peroxideanimal cellapoptosiscell differentiationcell proliferationthyroid cellcells, culturedthyroid gland

Abstract 

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 H 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 Plax I and Prx II reduces the amount of H2O2-induced apoptosis measured by these assays. These resuits 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.

ISSN 

0021-9258

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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