Osteoblast deletion of exon 3 of the androgen receptor gene results in trabecular bone loss in adult male mice

Amanda Notini, Julie McManus, Alison Moore, Mary Bouxsein, Mark Jimenez, W S Maria Chiu, Vaida Glatt, Barbara Kream, David Handelsman, Howard Morris, Jeffrey Zajac, Rachel Davey

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84 Citations (Scopus)


The mechanism of androgen action on bone was studied in male mice with the AR deleted in mature osteoblasts. These mice had decreased trabecular bone volume associated with a decrease in trabecular number, suggesting that androgens may act directly on osteoblasts to maintain trabecular bone. INTRODUCTION: Androgens modulate bone cell activity and are important for the maintenance of bone mass. However, the mechanisms by which they exert these actions on bone remain poorly defined. The aim of this study was to investigate the role of androgens acting through the classical androgen receptor (AR) signaling pathways (i.e., DNA-binding dependent pathways) in osteoblasts using male mice in which exon 3 of the AR gene was deleted specifically in mature osteoblasts. MATERIALS AND METHODS: Mice with a floxed exon 3 of the AR gene were bred with Col 2.3-cre transgenic mice, in which Cre recombinase is expressed in mineralizing osteoblasts. The skeletal phenotype of mutant mice was assessed by histomorphometry and quantitative microCT at 6, 12, and 32 weeks of age (n=8 per group). Wildtype, hemizygous exon 3 floxed and hemizygous Col 2.3-cre male littermates were used as controls. Data were analyzed by one-way ANOVA and Tukey s posthoc test. RESULTS: microCT analysis of the fifth lumbar vertebral body showed that these mice had reduced trabecular bone volume (p
Original languageEnglish
Pages (from-to)347 - 356
Number of pages10
JournalJournal of Bone and Mineral Research
Issue number3
Publication statusPublished - 2007
Externally publishedYes

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