Mol. Cells 2013; 36(3): 273-277
Published online September 17, 2014
https://doi.org/10.1007/s10059-013-0226-3
© The Korean Society for Molecular and Cellular Biology
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 mitogen-activated protein (MAP) kinase pathway suppressed induction of P2Y14 proteins. Extracellular addition of UDP-su-gars such as UDP-glucose, UDP-galactose, UDP-glucuro-nic 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.
Keywords osteoclastogenesis, P2Y14 receptor, RANKL, UDP-sugars
Mol. Cells 2013; 36(3): 273-277
Published online September 30, 2013 https://doi.org/10.1007/s10059-013-0226-3
Copyright © The Korean Society for Molecular and Cellular Biology.
Seung Ah Lee, Jin Hee Park, and Soo Young Lee
Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 120-750, Korea
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 mitogen-activated protein (MAP) kinase pathway suppressed induction of P2Y14 proteins. Extracellular addition of UDP-su-gars such as UDP-glucose, UDP-galactose, UDP-glucuro-nic 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.
Keywords: osteoclastogenesis, P2Y14 receptor, RANKL, UDP-sugars
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