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Androgen receptor knockout in ovarian theca cells results in altered steroidogenesis in diestrous female mice
Author(s) -
Tram Meilinn,
Andrisse Stanley,
Wolfe Andrew,
Wu Sheng
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1247.9
Subject(s) - endocrinology , medicine , theca , androgen receptor , estrous cycle , androgen , anovulation , polycystic ovary , theca interna , biology , ovary , vaginal smear , andrology , hormone , insulin resistance , insulin , prostate cancer , cancer
Approximately one out of ten women experience polycystic ovarian syndrome (PCOS). PCOS women exhibit hyperandrogenemia, oligo‐ or anovulation, and polycystic ovarian follicles. Females who exhibit elevated androgen levels have been shown to have reproductive abnormalities. However, it is unknown which target organs are impacted by elevated androgen levels . This study aims to determine the role of androgen receptors (AR) on steroidogenesis and the reproduction of female mice in ovarian theca cells. We utilized a cre‐lox model system to produce ovarian theca cell‐specific androgen receptor knockout (ThARKO) mice. ThARKO mice have dramatically reduced AR expression levels as assessed by both immunocytochemistry and real‐time qPCR. We also investigated age at puberty by assessing the age at vaginal opening and first estrus. There was no difference in the age at vaginal opening between control and ThARKO mice. There was also no significant difference in estrous cyclicity assessed by vaginal cytology. Ovaries of control and ThARKO mice were collected at diestrus and ovarian gene expression was compared in 2 month old mice. During diestrus, we observed an increased mRNA expression of cyp17 compared to control littermates. Cyp17 is the rate limiting step of androgen synthesis. Although fertility was not altered , the AR in theca cells may play a role in steroidogenesis. Support or Funding Information R00 DH056139, P60 DK079637, R01 HD068777