Bio: I have been recruited as INSERM researcher in 2007. I have then worked on the impact of Endocrine Disrupters (EDs) in order to understand how in utero and/or neonatal exposure could alter adult testicular physiology. Our data established SHP as a crucial mediator of the deleterious effect of estrogenic EDs, such as diethylstilbestrol, on testicular physiology. These effects seem to be driven through the regulation of the histone methyltransferase EHMT. Since 2010, we are now developing innovative thematic research to identify the molecular mechanisms underlying the links between liver disease (PH) and impaired male fertility. Our studies are mainly focused in understanding the role of the bile acid receptors FXRalpha and TGR5 in context of PH which are characterized bile increased plasma levels of bile acids. We are also interested in the impact of environment exposure such as endocrine disrupters (EDs) on testicular pathophysiology. We are mainly working on estrogen-like EDs in order to analyze their impact on spermatogenesis. The goal of our group is to better understand the mechanisms involved in generational transmission of anomalies leading to diseases such as altered development, obesity and/or diabetes.

Abstract: Male sexual function can be disrupted by exposure to exogenous compounds that cause testicular physiological alterations. The constitutive androstane receptor (Car) is a receptor for both endobiotics and xenobiotics involved in detoxification. However, its role in male fertility, particularly regarding the reprotoxic effects of environmental pollutants, remains unclear. This study aims to investigate the role of the Car signaling pathway in male fertility. In vivo, in vitro, and pharmacological approaches are utilized in wild-type and Car-deficient mouse models. The results indicate that Car inhibition impaired male fertility due to altered sperm quality, specifically histone retention, which is correlated with an increased percentage of dying offspring in utero. The data highlighted interactions among Car, Akt, Foxo1, and histone acetylation. This study demonstrates that Car is crucial in germ cell homeostasis and male fertility. Further research on the Car signaling pathway is necessary to reveal unidentified causes of altered fertility and understand the harmful impact of environmental molecules on male fertility and offspring health.