Defective circadian control in mesenchymal cells reduces adult bone mass in mice by promoting osteoclast function.

ABSTRACT: Serum bone turnover markers show diurnal variation in humans, suggesting that circadian rhythms contribute to normal bone physiology. This conclusion is corroborated by bone phenotypes in mice with genetic disruption of the circadian molecular clock mechanism, for instance via deletion of the transcription factor Brain and Muscle Arntl-like 1 (Bmal1). To dissect the contribution of circadian molecular clocks in individual bone cell types, we generated mice with conditional deletion of Bmal1 in osteoclasts (Ctsk-cre) and in mesenchymal cells of the limbs (Prx1-cre). We report that deletion of Bmal1 in osteoclasts had no effect on trabecular or cortical bone parameters in vivo or on osteoclast differentiation in vitro. In contrast, Bmal1^f/f.Prx1-cre mice had significantly less tra

SUBMITTER: Tsang K 

PROVIDER: S-EPMC6699618 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature