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This version published online on May 5, 2005
Endocrinology, doi:10.1210/en.2004-1619
A more recent version of this article appeared on August 1, 2005
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Submitted on December 16, 2004
Accepted on April 27, 2005

Transcriptional regulation of Dehydroepiandrosterone Sulfotransferase (SULT2A1) by Estrogen-Related Receptor {alpha} (ERR{alpha})

Jeremiah Seely, Karla Saner Amigh, Takashi Suzuki, Bobbie Mayhew, Hironobu Sasano, Vincent Giguere, Josée Laganière, Bruce R. Carr, and William E. Rainey*

Division of Reproductive Endocrinology and Infertility, UT Southwestern Medical Center, Dallas, Texas; McGill University Health Center, Montreal, Quebec; Tohoku University School of Medicine, Department of Pathology, Sendai, Japan

* To whom correspondence should be addressed. E-mail: william.rainey{at}utsouthwestern.edu.

The estrogen-related receptors (ERR {alpha}, {beta} and {gamma}) are a subfamily of orphan nuclear receptors (designated NR3B1, NR3B2 and NR3B3) that are structurally and functionally related to estrogen receptors {alpha} and {beta}. Herein we test the hypothesis that ERR{alpha} regulates transcription of the genes encoding the enzymes involved in adrenal steroid production. Real-time RT-PCR was first used to determine the levels of ERR{alpha} mRNA in various human tissues. Adult adrenal levels of ERR{alpha} transcript were similar to that seen in heart, which is known to highly express ERR{alpha}. Expression of ERR{alpha} in the adult adrenal was then confirmed using western blotting and immunohistochemistry. To examine the effects of ERR{alpha} on steroidogenic capacity we used reporter constructs with the 5'-flanking regions of steroidogenic acute regulatory protein (StAR), cholesterol side-chain cleavage (CYP11A), 3{beta} hydroxysteroid dehydrogenase type II (HSD3B2), 17{alpha} hydroxylase, 17,20 lyase (CYP17), and DHEA sulfotransferase (SULT2A1). Co-transfection of these reporter constructs with wild-type ERR{alpha} or VP16-ERR{alpha} expression vectors demonstrated ERR{alpha} enhanced reporter activity driven by flanking DNA from CYP17 and SULT2A1. SULT2A1 promoter activity was most responsive to the ERR{alpha} and VP16-ERR{alpha}, increasing activity 2.6- and 79.5-fold respectively. ERR{alpha} effects on SULT2A1 were greater than the stimulation seen in response to steroidogenic factor 1 (SF1). Transfection of serial deletions of the 5'-flanking DNA of the SULT2A1 gene and EMSA experiments indicated the presence of three functional regulatory cis-elements which shared sequence similarity to binding sites for SF1. Taken together, the expression of ERR{alpha} in the adrenal and its regulation of SULT2A1 suggest an important role for this orphan receptor in the regulation of adrenal steroid production.
Key words: adrenal • steroidogenesis • transcription factor • orphan nuclear receptor




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