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Murine Prostate Micro-dissection and Surgical Castration

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Dioxin causes ventral prostate agenesis by disrupting dorsoventral patterning in developing mouse prostate.

Chad M Vezina¹, Sarah Hicks Allgeier, Robert W Moore

¹School of Pharmacy, University of Wisconsin, Madison, Wisconsin 53705, USA.

Toxicological Sciences : an Official Journal of the Society of Toxicology

|September 10, 2008

Summary

In utero exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) disrupts prostate development by impairing the specification of ventral and dorsolateral prostatic buds. This disruption occurs via hyperactivation of aryl hydrocarbon receptor (AHR) signaling in the developing urogenital sinus.

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Identification, Histological Characterization, and Dissection of Mouse Prostate Lobes for In Vitro 3D Spheroid Culture Models

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Published on: September 18, 2018

Area of Science:

Developmental biology
Toxicology
Endocrinology

Background:

Prostate ductal development is androgen-dependent, originating from fetal urogenital sinus (UGS) mesenchyme and epithelium.
In utero exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is known to inhibit prostate budding.

Purpose of the Study:

To determine if TCDD inhibits the specification or initiation stage of prostatic bud formation.
To investigate the mechanism by which TCDD inhibits ventral and dorsolateral prostatic budding.

Main Methods:

Maternal TCDD exposure at specific embryonic stages (E14.5-16.5) to assess impact on ventral and dorsolateral prostatic bud formation.
Analysis of mesenchymal-epithelial signaling, aryl hydrocarbon receptor (AHR) and ARNT protein/mRNA expression, and AHR-dependent gene expression.
Histological examination of the UGS to identify potential barriers or altered signaling pathways.

Main Results:

TCDD exposure during critical specification windows (E15.5-16.5 for ventral, E14.5-15.5 for dorsolateral) maximally inhibited prostatic budding.
No smooth muscle barrier was found to block mesenchymal-epithelial signaling in the ventral prostate.
AHR, ARNT, and AHR-induced transcripts showed overlapping expression in the periprostatic mesenchyme, suggesting this as the site of TCDD action.
TCDD disrupted UGS dorsoventral patterning, altering prostatic bud specification and lobe formation.

Conclusions:

TCDD inhibits prostatic bud specification, not initiation, during critical developmental windows.
Hyperactivation of AHR signaling in the periprostatic mesenchyme disrupts UGS patterning and leads to ventral prostate agenesis.
Disrupted axial patterning offers a new model for understanding TCDD-induced developmental defects in the prostate and other organs.