Prenatally androgenized female rats develop uterine hyperplasia when adult

Mol Cell Endocrinol. 2020 Jan 1:499:110610. doi: 10.1016/j.mce.2019.110610. Epub 2019 Oct 4.

Abstract

Prenatal hyperandrogenization (PH) is hypothesized as one of the main factors contributing to the development of polycystic ovary syndrome (PCOS). In this study, we aimed to investigate the impact of prenatal exposure to androgen excess on the uterus when animals reach their adulthood. We found that PH altered the morphology of the uteri that show a hyperplastic morphology with increased total uterine thickness as well as luminal epithelium thickness, with both enhanced and altered distribution of glands as compared with controls. Morphological alterations were associated with an unbalanced homeostasis as assessed by the expression of regulators of cell cycle progression and cell death dynamics. PH also causes disturbances in the cell cycle of the uterine tissue and dysregulates cell death and survival pathways leading to the development of uterine hyperplasia. These findings suggest that PH may have a deleterious effect on the uterus.

Keywords: Endometrium; PCOS; Prenatal hyperandrogenism; Uterine.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Androgens / adverse effects*
  • Animals
  • Cell Cycle / drug effects
  • Cell Survival / drug effects
  • Disease Models, Animal
  • Female
  • Homeostasis / drug effects
  • Hyperplasia
  • Pregnancy
  • Prenatal Exposure Delayed Effects / chemically induced
  • Prenatal Exposure Delayed Effects / pathology*
  • Rats
  • Uterus / drug effects
  • Uterus / metabolism
  • Uterus / pathology*

Substances

  • Androgens