Bisphenol A induces COX-2 through the mitogen-activated protein kinase pathway and is associated with levels of inflammation-related markers in elderly populations
- Authors
- Song, Heewon; Park, Joonwoo; Bui, Phuong T. C.; Choi, KeunOh; Gye, Myung Chan; Hong, Yun-Chul; Kim, Jin Hee; Lee, Young Joo
- Issue Date
- Oct-2017
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Bisphenol A; Inflammation; COX-2 expression; Epidemiology
- Citation
- ENVIRONMENTAL RESEARCH, v.158, pp.490 - 498
- Indexed
- SCIE
SCOPUS
- Journal Title
- ENVIRONMENTAL RESEARCH
- Volume
- 158
- Start Page
- 490
- End Page
- 498
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/18735
- DOI
- 10.1016/j.envres.2017.07.005
- ISSN
- 0013-9351
- Abstract
- Bisphenol A (BPA) is a well-known endocrine-disrupting chemical, and it is one of the highest volume chemicals produced worldwide. Even though several in vivo and in vitro studies showed positive associations of BPA exposure with pro-inflammatory cytokines such as tumor necrosis factor-alpha and interleukin (IL)-6, the mechanism by which BPA induces inflammation is unclear. We investigated the mechanism by which BPA induces inflammation (expression of inflammation-related genes, changes in oxidative stress, and cell proliferation and migration) and evaluated the effect of BPA exposure on inflammation-related markers in epidemiologic studies using repeat urine and serum samples from elderly subjects. BPA induced COX-2 expression via nuclear translocation of NF-kappa B and activation of mitogen-activated protein kinase (MAPK) by phosphorylation of ERK1/2 and enhanced the migration of lung cancer A549 and breast cancer MDAMB-231 cells. In two epidemiologic studies, we detected associations of BPA with six inflammation -related markers (WBC, CRP, IL-10, ALT, AST, and gamma-GTP levels). Our findings probably suggest that BPA exposure induces inflammation and exacerbates tumorigenesis.
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