Androgens regulate ovarian follicular development by increasing follicle stimulating hormone receptor and <i>microRNA-125b</i> expression

  • Aritro Sen
    Division of Endocrinology and Metabolism, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642; and
  • Hen Prizant
    Division of Endocrinology and Metabolism, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642; and
  • Allison Light
    Division of Endocrinology and Metabolism, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642; and
  • Anindita Biswas
    Division of Endocrinology and Metabolism, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642; and
  • Emily Hayes
    Division of Endocrinology and Metabolism, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642; and
  • Ho-Joon Lee
    Center for Human Reproduction, New York, NY 10021
  • David Barad
    Center for Human Reproduction, New York, NY 10021
  • Norbert Gleicher
    Center for Human Reproduction, New York, NY 10021
  • Stephen R. Hammes
    Division of Endocrinology and Metabolism, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642; and

説明

<jats:title>Significance</jats:title> <jats:p> Androgens are primarily considered detrimental to women’s health. However, androgen-receptor KO mouse models have been used to establish that androgens are actually necessary for normal ovarian function and female fertility. Despite these observations, how androgens regulate female fertility is not known. Here we show that androgens promote follicular development via two mechanisms: ( <jats:italic>i</jats:italic> ) prevention of follicular atresia by inducing the expression of an antiapoptotic microRNA (miR), <jats:italic>miR-125b</jats:italic> ; and ( <jats:italic>ii</jats:italic> ) promotion of follicle growth by increasing follicle-stimulating hormone receptor levels in a transcription-independent fashion. These data considerably change our understanding of androgen effects in female reproduction, and help explain the ovarian physiology seen in patients with too little or too much androgen. </jats:p>

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