From the Cover: Lifelong Exposure of C57bl/6n Male Mice to Bisphenol A or Bisphenol S Reduces Recovery From a Myocardial Infarction.

Autor:	Kasneci A; Lady Davis Institute for Medical Research, Montréal, Québec H3T 1E2, Canada., Lee JS; Institut de Recherches Cliniques de Montréal, Montréal, Québec H2W 1R7, Canada., Yun TJ; Institut de Recherches Cliniques de Montréal, Montréal, Québec H2W 1R7, Canada., Shang J; Lady Davis Institute for Medical Research, Montréal, Québec H3T 1E2, Canada., Lampen S; Lady Davis Institute for Medical Research, Montréal, Québec H3T 1E2, Canada., Gomolin T; Lady Davis Institute for Medical Research, Montréal, Québec H3T 1E2, Canada., Cheong CC; Institut de Recherches Cliniques de Montréal, Montréal, Québec H2W 1R7, Canada.; Division of Experimental Medicine, Department of Medicine, McGill University, Montréal, Québec H3A 1A2, Canada., Chalifour LE; Lady Davis Institute for Medical Research, Montréal, Québec H3T 1E2, Canada.; Division of Experimental Medicine, Department of Medicine, McGill University, Montréal, Québec H3A 1A2, Canada.
Jazyk:	angličtina
Zdroj:	Toxicological sciences : an official journal of the Society of Toxicology [Toxicol Sci] 2017 Sep 01; Vol. 159 (1), pp. 189-202.
DOI:	10.1093/toxsci/kfx133
Abstrakt:	Bisphenol A (BPA) leaches from plastics to contaminate foodstuffs. Analogs, such as bisphenol S (BPS), are now used increasingly in manufacturing. Greater BPA exposure has been correlated with exacerbation of cardiovascular disease, including myocardial infarction (MI). To test the hypothesis that bisphenol exposure impairs cardiac healing, we exposed C57bl/6n mice to water containing 25ng/ml BPA or BPS from conception and surgically induced an MI in adult male progeny. Increased early death and cardiac dilation, and reduced cardiac function were found post-MI in BPA- and BPS-exposed mice. Flow cytometry revealed increased monocyte and macrophage infiltration that correlated with increased chemokine C-C motif ligand-2 expression in the infarct. In vitro BPA and BPS addition increased matrix metalloproteinase-9 (MMP) protein and secreted activity in RAW264.7 macrophage cells suggesting that invivo increases in MMP2 and MMP9 in exposed infarcts were myeloid-derived. Bone marrow-derived monocytes isolated from exposed mice had greater expression of pro-inflammatory polarization markers when chemokine stimulated indicating an enhanced susceptibility to develop a pro-inflammatory monocyte population. Chronic BPA exposure of estrogen receptor beta (ERβ) deficient mice did not worsen early death, cardiac structure/function, or expression of myeloid markers after an MI. In contrast, BPS exposure of ERβ-deficient mice resulted in greater death and expression of myeloid markers. We conclude that lifelong exposure to BPA or BPS augmented the monocyte/macrophage inflammatory response and adverse remodeling from an MI thereby reducing the ability to survive and successfully recover, and that the adverse effect of BPA, but not BPS, is downstream of ERβ signaling. (© The Author 2017. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.)
Databáze:	MEDLINE
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