Gene Expression in Porcine Bulbourethral Glands

TL;DR

This study investigates gene expression in pig bulbourethral glands during growth phases, finding that androgen signaling does not drive initial growth, possibly due to reduced estrogen inhibition.

Contribution

The study provides new insights into the hormonal regulation of bulbourethral gland growth in pigs, suggesting estrogen inhibition via GPER may drive growth during low hormone periods.

Findings

Androgen receptor and SRD5A2 gene expression remains low during initial allometric growth in late juvenile and prepuberal intervals.

Reduced estrogen synthesis may alleviate GPER-mediated growth inhibition, stimulating growth during low hormone periods.

Bulbourethral glands grow faster than the general body during late juvenile stages despite low androgen levels.

Abstract

Bulbourethral glands are a major accessory sex gland in the boar. Their rate of growth is similar to general body growth at 6 weeks of age, but subsequently, bulbourethral glands grow faster than the general body. This study evaluated the expression of two genes that would increase androgen signaling despite the relatively low androgen concentrations during this interval. Neither gene exhibited increased expression to provide an androgen-mediated stimulus for growth. Hence, the normally occurring reduction in endogenous estrogen synthesis, which would alleviate G protein-coupled estrogen receptor 1 (GPER)-mediated inhibition of growth, may be the cause for the initial stimulus of growth during this late juvenile interval.

The porcine bulbourethral glands produce a gel-type secretion. Although the role of these contributions to reproductive success remains murky, the bulbourethral glands are major accessory sex glands in this species. Isometric growth in the early neonatal interval is followed by allometric growth in the late juvenile interval (6 to 11 weeks of age), while circulating endogenous steroids are low. The rate of allometric growth increases during the peripuberal interval (16 to 20 weeks of age) when systemic testosterone is relatively high. Gene expression for androgen receptor (AR) and for the steroid 5 alpha-reductase 2 (SRD5A2) enzyme that synthesizes the more potent androgen dihydrotestosterone from its precursor was evaluated by qPCR analyses of bulbourethral gland tissue. Tissues were collected from control boars (2 weeks to 40 weeks of age) and from littermates of these boars treated with letrozole to suppress endogenous estrogen synthesis. Gene expression for these two key proteins in androgen signaling was quite low during the initial allometric growth in the late juvenile and prepuberal intervals, suggesting that this initial growth was not primarily stimulated by androgens. These observations are consistent with a more direct estrogen-mediated inhibition of growth via GPER previously proposed, with the sensitivity extending into the late juvenile interval when estrogens as well as androgens are normally relatively low.

Figures