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dc.contributor.authorWu, Yanguang
dc.contributor.authorBaumgarten, Sarah C.
dc.contributor.authorZhou, Ping
dc.contributor.authorStocco, Carlos
dc.date.accessioned2015-09-21T18:23:07Z
dc.date.available2015-09-21T18:23:07Z
dc.date.issued2013-08
dc.identifier.bibliographicCitationWu, Y. G., Baumgarten, S. C., Zhou, P. and Stocco, C. Testosterone-Dependent Interaction between Androgen Receptor and Aryl Hydrocarbon Receptor Induces Liver Receptor Homolog 1 Expression in Rat Granulosa Cells. Molecular and Cellular Biology. 2013. 33(15): 2817-2828. DOI: 10.1128/MCB.00011-13en_US
dc.identifier.issn0270-7306
dc.identifier.urihttp://hdl.handle.net/10027/19630
dc.descriptionThis is a copy of an article published in the Molecular and Cellular Biology © 2013 American Society for Microbiologyen_US
dc.description.abstractAndrogens play a major role in the regulation of normal ovarian function; however, they are also involved in the development of ovarian pathologies. These contrasting effects may involve a differential response of granulosa cells to the androgens testosterone (T) and dihydrotestosterone (DHT). To determine the molecular pathways that mediate the distinct effects of T and DHT, we studied the expression of the liver receptor homolog 1 (LRH-1) gene, which is differentially regulated by these steroids. We found that although both T and DHT stimulate androgen receptor (AR) binding to the LRH-1 promoter, DHT prevents T-mediated stimulation of LRH-1 expression. T stimulated the expression of aryl hydrocarbon receptor (AHR) and its interaction with the AR. T also promoted the recruitment of the AR/AHR complex to the LRH-1 promoter. These effects were not mimicked by DHT. We also observed that the activation of extracellular regulated kinases by T is required for AR and AHR interaction. In summary, T, but not DHT, stimulates AHR expression and the interaction between AHR and AR, leading to the stimulation of LRH-1 expression. These findings could explain the distinct response of granulosa cells to T and DHT and provide a molecular mechanism by which DHT negatively affects ovarian function.en_US
dc.description.sponsorshipThis work was supported by NIH grants R01HD057110 and R21HD066233en_US
dc.language.isoen_USen_US
dc.publisherAmerican Society for Microbiologyen_US
dc.subjectovaryen_US
dc.subjecttestosteroneen_US
dc.subjectDHTen_US
dc.subjectgranulosa cellsen_US
dc.titleTestosterone-Dependent Interaction between Androgen Receptor and Aryl Hydrocarbon Receptor Induces Liver Receptor Homolog 1 Expression in Rat Granulosa Cellsen_US
dc.typeArticleen_US


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