Chronic Estrus Disrupts Uterine Gland Development and Homeostasis

Author:

Stewart C Allison1,Stewart M David2,Wang Ying1,Mullen Rachel D1,Kircher Bonnie K1ORCID,Liang Rui2,Liu Yu2,Behringer Richard R1ORCID

Affiliation:

1. Department of Genetics, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA

2. Department of Biology and Biochemistry, University of Houston, Houston, Texas 77004, USA

Abstract

Abstract Female mice homozygous for an engineered Gnrhr E90K mutation have reduced gonadotropin-releasing hormone signaling, leading to infertility. Their ovaries have numerous antral follicles but no corpora lutea, indicating a block to ovulation. These mutants have high levels of circulating estradiol and low progesterone, indicating a state of persistent estrus. This mouse model provided a unique opportunity to examine the lack of cyclic levels of ovarian hormones on uterine gland biology. Although uterine gland development appeared similar to controls during prepubertal development, it was compromised during adolescence in the mutants. By age 20 weeks, uterine gland development was comparable to controls, but pathologies, including cribriform glandular structures, were observed. Induction of ovulations by periodic human chorionic gonadotropin treatment did not rescue postpubertal uterine gland development. Interestingly, progesterone receptor knockout mice, which lack progesterone signaling, also have defects in postpubertal uterine gland development. However, progesterone treatment did not rescue postpubertal uterine gland development. These studies indicate that chronically elevated levels of estradiol with low progesterone and therefore an absence of cyclic ovarian hormone secretion disrupts postpubertal uterine gland development and homeostasis.

Funder

National Institutes of Health

American Heart Association

University of Houston Division of Research

Publisher

The Endocrine Society

Subject

Endocrinology

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