Abstract
The purinergic receptor P2Y, G protein coupled, 14 (P2Y14) receptor for UDP-glucose and other UDP-sugars has been implicated in the regulation of the stem cell compartment as well as neuroimmune function. However, the role of P2Y14 in osteoclast formation is completely unknown. We found that RANKL selectively induced P2Y14 among seven mammalian P2Y receptors when analysed at both the mRNA and protein level, but inhibitors of the mitogenactivated protein (MAP) kinase pathway suppressed induction of P2Y14 proteins. Extracellular addition of UDP-sugars such as UDP-glucose, UDP-galactose, UDP-glucuronic acid, and UDP-N-acetyl glucosamine promoted RANKL- induced osteoclastogenesis, while P2Y14 downregulation by RNA interference inhibited osteoclast formation. Taken together, these results suggest that P2Y14 may act as the receptor for UDP-sugars in osteoclast precusors and may regulate RANKL-induced osteoclastogenesis.
Original language | English |
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Pages (from-to) | 273-277 |
Number of pages | 5 |
Journal | Molecules and Cells |
Volume | 36 |
Issue number | 3 |
DOIs | |
State | Published - Sep 2013 |
Bibliographical note
Funding Information:This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea Government [(Ministry of Science, ICT and Future Planning (MSIP); No. 201 3R 1A2A1A05005153; No. 2012R1A5A1048236; No. 2012M3A9C 5048708)]. S.L. and J.P. were supported by the second stage of the Brain Korea 21 Project.
Keywords
- Osteoclastogenesis
- P2Y14 receptor
- RANKL
- UDP-sugars