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Role of Androgen and Estrogen Receptors for the Action of Dehydroepiandrosterone (DHEA)

Artikel i vetenskaplig tidskrift
Författare Cecilia Engdahl
Marie K Lagerquist
Alexandra Stubelius
Annica Andersson
Erik Studer
Claes Ohlsson
Lars Westberg
Hans Carlsten
Helena Forsblad d'Elia
Publicerad i Endocrinology
Volym 155
Nummer/häfte 3
Sidor 889-896
ISSN 0013-7227
Publiceringsår 2014
Publicerad vid Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning
Centre for Bone and Arthritis Research
Institutionen för neurovetenskap och fysiologi, sektionen för farmakologi
Institutionen för medicin, avdelningen för invärtesmedicin och klinisk nutrition
Sidor 889-896
Språk en
Länkar dx.doi.org/10.1210/en.2013-1561
https://gup.ub.gu.se/file/127115
Ämnesord PRIMARY SJOGRENS-SYNDROME, SUBMANDIBULAR-GLANDS, MALE-MICE, CORTICAL, BONE, ACTIVATION, CELL, HORMONE, BINDING, PROTEIN, ALPHA
Ämneskategorier Endokrinologi

Sammanfattning

Dehydroepiandrosterone (DHEA) is an abundant steroid hormone, and its mechanism of action is yet to be determined. The aim of this study was to elucidate the importance of androgen receptors (ARs) and estrogen receptors (ERs) for DHEA function. Orchidectomized C57BL/6 mice were treated with DHEA, DHT, 17 beta-estradiol-3-benzoate (E2), or vehicle. Orchidectomized AR-deficient (ARKO) mice and wild-type (WT) littermates were treated with DHEA or vehicle for 2.5 weeks. At termination, bone mineral density (BMD) was evaluated, thymus and seminal vesicles were weighted, and submandibular glands (SMGs) were histologically examined. To evaluate the in vivo ER activation of the classical estrogen signaling pathway, estrogen response element reporter mice were treated with DHEA, DHT, E2, or vehicle, and a reporter gene was investigated in different sex steroid-sensitive organs after 24 hours. DHEA treatment increased trabecular BMD and thymic atrophy in both WT and ARKO mice. In WT mice, DHEA induced enlargement of glands in the SMGs, whereas this effect was absent in ARKO mice. Furthermore, DHEA was able to induce activation of classical estrogen signaling in bone, thymus, and seminal vesicles but not in the SMGs. In summary, the DHEA effects on trabecular BMD and thymus do not require signaling via AR and DHEA can activate the classical estrogen signaling in these organs. In contrast, DHEA induction of gland size in the SMGs is dependent on AR and does not involve classical estrogen signaling. Thus, both ERs and ARs are involved in mediating the effects of DHEA in an organ-dependent manner.

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