1. Peroxisome proliferator-activated receptor-binding protein null mutation results in defective mammary gland development.
- Author
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Jia Y, Qi C, Zhang Z, Zhu YT, Rao SM, and Zhu YJ
- Subjects
- Animals, Bromodeoxyuridine pharmacology, Caseins metabolism, Cell Proliferation, Epithelial Cells cytology, Estrogens metabolism, Genotype, Lactation, Mammary Glands, Animal embryology, Mammary Glands, Animal metabolism, Mediator Complex Subunit 1, Mice, Milk Proteins metabolism, Models, Genetic, Oligonucleotide Array Sequence Analysis, Progesterone metabolism, RNA metabolism, RNA, Messenger metabolism, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, Time Factors, Transgenes, Mutation, Transcription Factors genetics
- Abstract
A conditional null mutation of peroxisome proliferator-activated receptor-binding protein (PBP) gene was generated to understand its role in mammary gland development. PBP-deficient mammary glands exhibited retarded ductal elongation during puberty, and decreased alveolar density during pregnancy and lactation. PBP-deficient mammary glands could not produce milk to nurse pups during lactation. Both the mammary ductal elongation in response to estrogen treatment and the mammary lobuloalveolar proliferation stimulated by estrogen plus progesterone were attenuated in PBP-deficient mammary glands. The proliferation index was decreased in PBP-deficient mammary glands. PBP-deficient mammary epithelial cells expressed abundant beta-casein, whey acidic protein, and WDNM1 mRNA, indicating a relatively intact differentiated function. PBP-deficient epithelial cells were unable to form mammospheres, which were considered to be derived from mammary progenitor/stem cells. We conclude that PBP plays a pivotal role in the normal mammary gland development.
- Published
- 2005
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