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Sci Rep. 2017 Aug 30;7(1):9925. doi: 10.1038/s41598-017-09793-y.

Transforming Growth Factor Beta is regulated by a Glucocorticoid-Dependent Mechanism in Denervation Mouse Bone.

Author information

1
School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, China.
2
Department of Chinese Medicine, Guangzhou General Hospital of Guangzhou Command, PLA, Guangzhou, China.
3
Department of Neurology, University of Chicago, Chicago, IL, USA.
4
College of Dentistry, University of New York, New York, NY, USA.
5
School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, China. lijinlong@smu.edu.cn.
6
Department of Neurology, University of Chicago, Chicago, IL, USA. sunxn263@hotmail.com.
7
School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, China. dhy48321@smu.edu.cn.

Abstract

Bone growth and remodeling is inhibited by denervation in adults and children, resulting in alterations of linear growth and bone mass and increased risk for osteoporosis and pathologic fractures. Transforming growth factor beta (TGF-β) isoforms are a key group of growth factors that enhance bone formation. To explore the relation between denervation-induced reduction of bone formation and TGF-β gene expression, we measured mRNA levels of TGF-β in denervation mouse bone and found decreased mRNA levels of TGF-β1, TGF-β2 and TGF-β3. These changes were accompanied by diminishing weight loss, bone mineral density (BMD), trabecular thickness, trabecular separation and trabecular number of femur and lumbar, serum osteocalcin, total calcium, intact parathyroid hormone, and increased serum C telopeptide. Recombinant human TGF-β1 (rhTGF-β1) prevented denervation-induced reduction of BMD further supporting our hypothesis that denervation-induced reduction of bone formation is a result of inhibition of TGF-β gene expression. In addition, antiprogestins RU 38486 blunted the denervation-induced decrease in mRNA levels of TGF-β group, while dexamethasone (DEX) decreased TGF-β group mRNA levels in normal mice. Furthermore, the denervated-mice exhibited a threefold increase in plasma corticosterone. These results suggest that denervation-induced reduction of bone formation may be regulated by glucocorticoids via inhibition of TGF-β gene expression at least in part.

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