The mechanism of oxytocin and its receptors in regulating cells in bone metabolism

Frontiers in Pharmacology

Pharmacology

Miao Jinxin¹  Zhang Yunke²  Li Xiang³  Lin Zixuan⁴  Liu Feixiang⁴  Wang Jianru⁴  Feng Yanchen⁵ 

[1] Research and Experiment Center, Henan University of Chinese Medicine, Zhengzhou, China;School of Rehabilitation Medicine, Henan University of Chinese Medicine, Zhengzhou, China;State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China;Research Units of Infectious Disease and Microecology, Chinese Academy of Medical Sciences, Hangzhou, China;The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, Henan, China;Traditional Chinese Medicine (Zhong Jing) School, Henan University of Chinese Medicine, Zhengzhou, Henan, China;

关键词: immune inflammation;    epigenetics;    oxytocin;    oxytocin receptor;    osteoporosis;    estrogen;    bone marrow mesenchymal stem cells;    osteoblasts;   

DOI  :  10.3389/fphar.2023.1171732

 received in 2023-02-22, accepted in 2023-04-20,  发布年份 2023

来源: Frontiers

【 摘 要 】

Oxytocin (OT) is a neuropeptide known to affect social behavior and cognition. The epigenetic modification of the oxytocin receptor (OTR) via DNA methylation stimulates parturition and breast milk secretion and inhibits craniopharyngioma, breast cancer, and ovarian cancer growth significantly as well as directly regulates bone metabolism in their peripheral form rather than the central form. OT and OTR can be expressed on bone marrow mesenchymal stem cells (BMSCs), osteoblasts (OB), osteoclasts (OC), osteocytes, chondrocytes, and adipocytes. OB can synthesize OT under the stimulation of estrogen as a paracrine–autocrine regulator for bone formation. OT/OTR, estrogen, and OB form a feed-forward loop through estrogen mediation. The osteoclastogenesis inhibitory factor (OPG)/receptor activator of the nuclear factor kappa-B ligand (RANKL) signaling pathway is crucially required for OT and OTR to exert anti-osteoporosis effect. Downregulating the expression of bone resorption markers and upregulating the expression of the bone morphogenetic protein, OT could increase BMSC activity and promote OB differentiation instead of adipocytes. It could also stimulate the mineralization of OB by motivating OTR translocation into the OB nucleus. Moreover, by inducing intracytoplasmic Ca2+ release and nitric oxide synthesis, OT could regulate the OPG/RANKL ratio in OB and exert a bidirectional regulatory effect on OC. Furthermore, OT could increase the activity of osteocytes and chondrocytes, which helps increase bone mass and improve bone microstructure. This paper reviews recent studies on the role of OT and OTR in regulating cells in bone metabolism as a reference for their clinical use and research based on their reliable anti-osteoporosis effects.

【 授权许可】

Unknown   
Copyright © 2023 Feixiang, Yanchen, Xiang, Yunke, Jinxin, Jianru and Zixuan.