Sphingosylphosphorylcholine blocks ovariectomy-induced bone loss by suppressing Ca


Journal

Journal of cellular and molecular medicine
ISSN: 1582-4934
Titre abrégé: J Cell Mol Med
Pays: England
ID NLM: 101083777

Informations de publication

Date de publication:
01 2021
Historique:
received: 31 03 2020
revised: 29 09 2020
accepted: 01 11 2020
pubmed: 25 11 2020
medline: 1 10 2021
entrez: 24 11 2020
Statut: ppublish

Résumé

Osteoporosis is a disease in which bone mineral density decreases due to abnormal activity of osteoclasts, and is commonly found in post-menopausal women who have decreased levels of female hormones. Sphingosylphosphorylcholine (SPC) is an important biological lipid that can be converted to sphingosine-1-phosphate (S1P) by autotaxin. S1P is known to be involved in osteoclast activation by stimulating osteoblasts, but bone regulation by SPC is not well understood. In this study, we found that SPC strongly inhibits RANKL-induced osteoclast differentiation. SPC-induced inhibitory effects on osteoclast differentiation were not affected by several antagonists of S1P receptors or pertussis toxin, suggesting cell surface receptor independency. However, SPC inhibited RANKL-induced calcineurin activation and subsequent NFATc1 activity, leading to decrease of the expression of Trap and Ctsk. Moreover, we found that bone loss in an experimental osteoporosis mouse model was recovered by SPC injection. SPC also blocked ovariectomy-induced body weight increase and Nfatc1 gene expression in mice. We also found that SPC inhibits RANKL-induced osteoclast differentiation in human macrophages. Since currently available treatments for osteoporosis, such as administration of female hormones or hormone receptor modulators, show serious side effects, SPC has potential as a new agent for osteoporosis treatment.

Identifiants

pubmed: 33230972
doi: 10.1111/jcmm.16101
pmc: PMC7810965
doi:

Substances chimiques

Calmodulin 0
sphingosine phosphorylcholine 10216-23-6
Phosphorylcholine 107-73-3
Sphingosine NGZ37HRE42
Calcium SY7Q814VUP

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

473-483

Subventions

Organisme : National Research Foundation of Korea
ID : NRF-2017R1A5A1014560
Organisme : National Research Foundation of Korea
ID : NRF-2018R1A2B3003868

Informations de copyright

© 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.

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Auteurs

Ha Young Lee (HY)

Department of Biological Sciences, Sungkyunkwan University, Suwon, Korea.

Kwang Min Cho (KM)

Department of Biological Sciences, Sungkyunkwan University, Suwon, Korea.

Min Kyung Kim (MK)

Department of Cell and Developmental Biology, BK21 Program and Dental Research Institute, Seoul National University, Seoul, Korea.

Mingyu Lee (M)

Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, Korea.

Hun Kim (H)

Department of Precision Medicine, Institute for Antimicrobial Resistance Research and Therapeutics, Sungkyunkwan University School of Medicine, Suwon, Korea.

Cheol Yong Choi (CY)

Department of Biological Sciences, Sungkyunkwan University, Suwon, Korea.

Kyeong Kyu Kim (KK)

Department of Precision Medicine, Institute for Antimicrobial Resistance Research and Therapeutics, Sungkyunkwan University School of Medicine, Suwon, Korea.

Joon Seong Park (JS)

Department of Hematology-Oncology, Ajou University School of Medicine, Suwon, Korea.

Hong-Hee Kim (HH)

Department of Cell and Developmental Biology, BK21 Program and Dental Research Institute, Seoul National University, Seoul, Korea.

Yoe-Sik Bae (YS)

Department of Biological Sciences, Sungkyunkwan University, Suwon, Korea.
Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, Korea.

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Classifications MeSH