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This version published online on July 20, 2006
Endocrinology, doi:10.1210/en.2006-0437
A more recent version of this article appeared on October 1, 2006
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Submitted on April 6, 2006
Accepted on July 11, 2006

PPAR{alpha} Activation During Pregnancy Severely Impairs Mammary Lobuloalveolar Development in Mice

Qian Yang, Reiko Kurotani, Atsushi Yamada, Shioko Kimura, and Frank J. Gonzalez*

Laboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892

* To whom correspondence should be addressed. E-mail: fjgonz{at}helix.nih.gov.

To identify the potential functions of peroxisome proliferator-activated receptor alpha (PPAR{alpha}) in skin development, transgenic mice were generated to target constitutively activated PPAR{alpha} (VP16PPAR{alpha}) to the stratified epithelia by use of the keratin K5 promoter. In addition to marked alterations in epidermal development, the transgenic mice had a severe defect in lactation during pregnancy resulting in 100% pup mortality. In this study, the alteration of mammary gland development in these transgenic mice was investigated. The results showed that expression of the VP16PPAR{alpha} transgene during pregnancy resulted in impaired development of lobuloalveoli, which is associated with reduced proliferation and increased apoptosis of mammary epithelia. Mammary epithelia from transgenic mice also showed a significant reduction in the expression of {beta}-catenin and a down-regulation of one of its target genes, cyclin D1, which is thought to be required for lobuloalveolar development. Furthermore, upon PPAR{alpha} ligand treatment, similar effects on lobuloalveolar development were observed in wild-type mice, but not in PPAR{alpha}-null mice. These findings suggest that PPAR{alpha} activation has a marked influence in mammary lobuloalveolar development.
Key words: VP16PPAR{alpha} • mammary gland • lobuloalveoli • lactation • cyclin D1 • {beta}-catenin




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