Bisphenol S causes excessive estrogen synthesis by activating FSHR and the downstream cAMP/PKA signaling pathway.

Autor: Zhang X; College of Marine Life Sciences, Ocean University of China, 266003, Qingdao, Shandong Province, China.; Tai'an Agriculture and Rural Affairs Bureau, 271000, Tai'an, Shandong Province, China., Zhang X; College of Marine Life Sciences, Ocean University of China, 266003, Qingdao, Shandong Province, China., Zhang Z; College of Marine Life Sciences, Ocean University of China, 266003, Qingdao, Shandong Province, China., Shi Y; College of Marine Life Sciences, Ocean University of China, 266003, Qingdao, Shandong Province, China., Wang J; College of Marine Life Sciences, Ocean University of China, 266003, Qingdao, Shandong Province, China., Ru S; College of Marine Life Sciences, Ocean University of China, 266003, Qingdao, Shandong Province, China., Tian H; College of Marine Life Sciences, Ocean University of China, 266003, Qingdao, Shandong Province, China. tianhua@ouc.edu.cn.
Jazyk: angličtina
Zdroj: Communications biology [Commun Biol] 2024 Jul 10; Vol. 7 (1), pp. 844. Date of Electronic Publication: 2024 Jul 10.
DOI: 10.1038/s42003-024-06449-2
Abstrakt: Estrogen excess in females has been linked to a diverse array of chronic and acute diseases. Emerging research shows that exposure to estrogen-like compounds such as bisphenol S leads to increases in 17β-estradiol levels, but the mechanism of action is unclear. The aim of this study was to reveal the underlying signaling pathway-mediated mechanisms, target site and target molecule of action of bisphenol S causing excessive estrogen synthesis. Human ovarian granulosa cells SVOG were exposed to bisphenol S at environmentally relevant concentrations (1 μg/L, 10 μg/L, and 100 μg/L) for 48 h. The results confirms that bisphenol S accumulates mainly on the cell membrane, binds to follicle stimulating hormone receptor (FSHR) located on the cell membrane, and subsequently activates the downstream cyclic adenosine monophosphate/protein kinase A (cAMP/PKA) signaling pathway, leading to enhanced conversion of testosterone to 17β-estradiol. This study deepens our knowledge of the mechanisms of environmental factors in pathogenesis of hyperestrogenism.
(© 2024. The Author(s).)
Databáze: MEDLINE
Externí odkaz:
Nepřihlášeným uživatelům se plný text nezobrazuje