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BPA-Toxicity via Superoxide Anion Overload and a Deficit in beta-Catenin Signaling in Human Bone Mesenchymal Stem Cells

Title
BPA-Toxicity via Superoxide Anion Overload and a Deficit in beta-Catenin Signaling in Human Bone Mesenchymal Stem Cells
Authors
Leem, Yea-HyunOh, SeikwanKang, Hong-JeKim, Jung-HwaYoon, JunoChang, Jae-Suk
Ewha Authors
오세관임예현
SCOPUS Author ID
오세관scopus; 임예현scopus
Issue Date
2017
Journal Title
ENVIRONMENTAL TOXICOLOGY
ISSN
1520-4081JCR Link1522-7278JCR Link
Citation
vol. 32, no. 1, pp. 344 - 352
Keywords
bisphenol Asuperoxide dismutaseMnTBAPhuman bone mesenchymal stem cellsbeta-cateninGSK3 beta
Publisher
WILEY-BLACKWELL
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Bisphenol A (BPA), used in the manufacture of products based on polycarbonate plastics and epoxy resins, is well known as an endocrine-disrupting monomer. In the current study, BPA increased cytotoxicity in hBMSCs in a dose-and time-dependent manner, concomitantly with increased lipid peroxidation. Increased cell death in BPA-treated cells was markedly blocked by pretreatment with the superoxide dismutase mimetic MnTBAP and MnTMPyP, but not by catalase, glutathione, the glutathione peroxidase mimetic ebselen, the NOS inhibitor NAME, or the xanthine oxidase inhibitor allopurinol. Furthermore, the decline in nuclear beta-catenin and cyclin D1 levels in hBMSCs exposed to BPA was reversed by MnTBAP treatment. Finally, treatment of hBMSCs with the GSK3 beta inhibitor LiCl2 increased nuclear beta-catenin levels and significantly attenuated cytotoxicity compared with BPA treatment. Our current results in hBMSCs exposed to BPA suggest that BPA causes a disturbance in beta-catenin signaling via a superoxide anion overload. (C) 2016 The Authors Environmental Toxicology Published by Wiley Periodicals, Inc.
DOI
10.1002/tox.22239
Appears in Collections:
의학전문대학원 > 의학과 > Journal papers
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