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Related Experiment Videos

Androgens Modulate Rat Granulosa Cell Steroidogenesis.

Manuel Doblado1, Lingzhi Zhang1, Tannaz Toloubeydokhti1

  • 1Division of Reproductive Endocrinology and Infertility, Department of Obstetrics, Gynecology & Reproductive Sciences, University of California, San Diego, 9500 Gilman Drive, 0633, La Jolla, San Diego, CA, 92093-0633, USA.

Reproductive Sciences (Thousand Oaks, Calif.)
|January 10, 2020
PubMed
Summary

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Androgens, like testosterone (T) and 5-alpha-dihydrotestosterone (DHT), stimulate progesterone production in ovarian granulosa cells (GCs). This occurs through direct action on androgen receptors and estrogen receptor-mediated effects, impacting follicular steroidogenesis.

Area of Science:

  • Reproductive biology
  • Endocrinology
  • Cellular signaling

Background:

  • Paracrine signaling between theca-interstitial cells (TICs) and granulosa cells (GCs) is crucial for ovarian follicular steroidogenesis.
  • Androgens, produced by TICs, influence GC function and serve as precursors for estrogen synthesis.

Purpose of the Study:

  • To investigate the impact of TIC co-culture and specific androgens (testosterone [T], 5-alpha-dihydrotestosterone [DHT]) on GC gene expression related to progesterone synthesis.
  • To elucidate the roles of testosterone (T), 5-alpha-dihydrotestosterone (DHT), and estradiol (E2) in modulating GC progesterone production pathways.

Main Methods:

  • Primary granulosa cells (GCs) from immature rats were cultured with or without TICs, DHT, or T.
  • Quantitative real-time PCR (qt-PCR) was used to analyze the expression of Hsd3b and Cyp11 genes in GCs.
Keywords:
AndrogensGene expressionGranulosa cellsRat

Related Experiment Videos

  • Hormone concentrations in spent media were measured, and the effects of anti-androgens and anti-estrogens were assessed.
  • Main Results:

    • Co-culture with TICs significantly upregulated Hsd3b and Cyp11 expression in GCs.
    • DHT and T treatment resulted in a dose-dependent increase in Hsd3b and Cyp11 expression and progesterone levels.
    • Estradiol (E2) also enhanced Hsd3b and Cyp11 expression, with androgen effects being blocked by anti-androgen and anti-estrogen treatments.

    Conclusions:

    • Androgens directly upregulate progesterone production in GCs by influencing key genes (Hsd3b, Cyp11).
    • These androgenic effects are mediated through both androgen receptors and estrogen receptors, highlighting a complex regulatory network.
    • Understanding these paracrine interactions is vital for comprehending follicular steroidogenesis and reproductive health.