Prostaglandin E2 mediates sensory nerve regulation of bone homeostasis

Hao Chen, Bo Hu, Xiao Lv, Shouan Zhu, Gehua Zhen, Mei Wan, Amit Jain, Bo Gao, Yu Chai, Mi Yang, Xiao Wang, Ruoxian Deng, Lei Wang, Yong Cao, Shuangfei Ni, Shen Liu, Wen Yuan, Huajiang Chen, Xinzhong Dong, Yun Guan, Huilin Yang () and Xu Cao ()
Additional contact information
Hao Chen: The Johns Hopkins University
Bo Hu: The Johns Hopkins University
Xiao Lv: The Johns Hopkins University
Shouan Zhu: The Johns Hopkins University
Gehua Zhen: The Johns Hopkins University
Mei Wan: The Johns Hopkins University
Amit Jain: The Johns Hopkins University
Bo Gao: The Johns Hopkins University
Yu Chai: The Johns Hopkins University
Mi Yang: The Johns Hopkins University
Xiao Wang: The Johns Hopkins University
Ruoxian Deng: The Johns Hopkins University
Lei Wang: The Johns Hopkins University
Yong Cao: The Johns Hopkins University
Shuangfei Ni: The Johns Hopkins University
Shen Liu: The Johns Hopkins University
Wen Yuan: Second Military Medical University
Huajiang Chen: Second Military Medical University
Xinzhong Dong: The Johns Hopkins University School of Medicine
Yun Guan: The Johns Hopkins University School of Medicine
Huilin Yang: First Affiliated Hospital of Soochow University
Xu Cao: The Johns Hopkins University

Nature Communications, 2019, vol. 10, issue 1, 1-13

Abstract: Abstract Whether sensory nerve can sense bone density or metabolic activity to control bone homeostasis is unknown. Here we found prostaglandin E2 (PGE2) secreted by osteoblastic cells activates PGE2 receptor 4 (EP4) in sensory nerves to regulate bone formation by inhibiting sympathetic activity through the central nervous system. PGE2 secreted by osteoblasts increases when bone density decreases as demonstrated in osteoporotic animal models. Ablation of sensory nerves erodes the skeletal integrity. Specifically, knockout of the EP4 gene in the sensory nerves or cyclooxygenase-2 (COX2) in the osteoblastic cells significantly reduces bone volume in adult mice. Sympathetic tone is increased in sensory denervation models, and propranolol, a β2-adrenergic antagonist, rescues bone loss. Furthermore, injection of SW033291, a small molecule to increase PGE2 level locally, significantly boostes bone formation, whereas the effect is obstructed in EP4 knockout mice. Thus, we show that PGE2 mediates sensory nerve to control bone homeostasis and promote regeneration.

Date: 2019
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DOI: 10.1038/s41467-018-08097-7

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