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Mol Cells. 2013 Sep;36(3):273-7. doi: 10.1007/s10059-013-0226-3. Epub 2013 Sep 17.

Selective induction of P2Y14 receptor by RANKL promotes osteoclast formation.

Author information

1
Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul, 120-750, Korea.

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.

PMID:
24048691
PMCID:
PMC3887970
DOI:
10.1007/s10059-013-0226-3
[Indexed for MEDLINE]
Free PMC Article

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