Prenatal Androgenization Alters the Development of GnRH Neuron and Preoptic Area RNA Transcripts in Female Mice

Author:

Burger Laura L1ORCID,Wagenmaker Elizabeth R1,Phumsatitpong Chayarndorn1ORCID,Olson David P12ORCID,Moenter Suzanne M134ORCID

Affiliation:

1. Department of Molecular and Integrative Physiology, Ann Arbor, Michigan

2. Department of Pediatrics, Ann Arbor, Michigan

3. Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan

4. Department of Obstetrics and Gynecology, University of Michigan, Ann Arbor, Michigan

Abstract

Abstract Polycystic ovary syndrome (PCOS) is the most common form of infertility in women. The causes of PCOS are not yet understood and both genetics and early-life exposure have been considered as candidates. With regard to the latter, circulating androgens are elevated in mid–late gestation in women with PCOS, potentially exposing offspring to elevated androgens in utero; daughters of women with PCOS are at increased risk for developing this disorder. Consistent with these clinical observations, prenatal androgenization (PNA) of several species recapitulates many phenotypes observed in PCOS. There is increasing evidence that symptoms associated with PCOS, including elevated luteinizing hormone (LH) (and presumably gonadotropin-releasing hormone [GnRH]) pulse frequency emerge during the pubertal transition. We utilized translating ribosome affinity purification coupled with ribonucleic acid (RNA) sequencing to examine GnRH neuron messenger RNAs from prepubertal (3 weeks) and adult female control and PNA mice. Prominent in GnRH neurons were transcripts associated with protein synthesis and cellular energetics, in particular oxidative phosphorylation. The GnRH neuron transcript profile was affected more by the transition from prepuberty to adulthood than by PNA treatment; however, PNA did change the developmental trajectory of GnRH neurons. This included families of transcripts related to both protein synthesis and oxidative phosphorylation, which were more prevalent in adults than in prepubertal mice but were blunted in PNA adults. These findings suggest that prenatal androgen exposure can program alterations in the translatome of GnRH neurons, providing a mechanism independent of changes in the genetic code for altered expression.

Funder

National Institutes of Health

Eunice Kennedy Shriver National Institute of Child Health and Human Development

Publisher

The Endocrine Society

Subject

Endocrinology

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