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Published on: July 24, 2017
TCDD exposure disrupts mammary epithelial cell differentiation and function.
Loretta L Collins1, Betina J Lew, B Paige Lawrence
1Department of Environmental Medicine, School of Medicine and Dentistry, University of Rochester, 601 Elmwood Avenue, Rochester, NY, USA.
Reproductive Toxicology (Elmsford, N.Y.)
|June 4, 2009
Summary
2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure disrupts mammary gland development and function by activating the aryl hydrocarbon receptor (AhR). This environmental contaminant impairs cell structure and reduces key protein production, impacting mammary epithelial cell differentiation.
Area of Science:
- Environmental Toxicology
- Developmental Biology
- Cell Biology
Background:
- Mammary gland development is crucial during pregnancy and is sensitive to environmental toxins.
- 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a persistent environmental contaminant and a potent aryl hydrocarbon receptor (AhR) agonist.
- TCDD exposure can interfere with normal physiological processes.
Purpose of the Study:
- To investigate the effects of TCDD on mammary gland growth and differentiation.
- To explore the molecular mechanisms underlying TCDD's impact on mammary epithelial cells.
- To establish an in vitro model for studying TCDD's effects on mammary epithelial cell function.
Main Methods:
- Exposure of pregnant mice and cultured SCp2 mammary epithelial cells to TCDD.
- Assessment of beta-casein protein induction.
- Evaluation of cell morphology, clustering, and alveolar-like structure formation.
- Analysis of AhR target gene (CYP1B1) expression.
- Measurement of E-cadherin expression and STAT5 phosphorylation.
Main Results:
- TCDD exposure reduced beta-casein protein induction in vivo and in vitro.
- SCp2 cells showed impaired cell clustering and reduced alveolar-like structure formation upon TCDD exposure.
- TCDD induced CYP1B1 expression, confirming AhR activation.
- Mammary glands exhibited reduced E-cadherin expression and decreased STAT5 phosphorylation following TCDD exposure during pregnancy.
Conclusions:
- TCDD-mediated AhR activation disrupts the structural and functional differentiation of the mammary gland.
- TCDD interferes with key molecular pathways regulating mammary epithelial cell function, including cell adhesion and signaling.
- The study presents a valuable in vitro model for further investigation of TCDD's toxicological effects on mammary epithelial cells.
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