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. 2019 Jan 1;8(1):17. doi: 10.3390/cells8010017

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Inhibition of S1PR2 by its specific antagonist (JTE013) attenuated Nfatc1, Ctsk, Acp5, Oscar, Dc-stamp, and Oc-stamp mRNA expressions induced by RANKL with or without co-culture with Aa-stimulated cell culture media. Murine BMs were treated with vehicle or JTE013. Cell were either unstimulated, cultured with Aa-stimulated cell culture media (Aa-media) alone, RANKL alone, or co-cultured with both RANKL and Aa-media as described in Methods. (A) Nfatc1 mRNA, (B) Ctsk mRNA, (C) Acp5 mRNA, (D) Oscar mRNA, (E) Dc-stamp mRNA, (F) Oc-stamp mRNA, (G) RANKL mRNA, and (H) OPG mRNA levels were quantified by real time PCR and normalized by GAPDH expression. (* p < 0.05, *** p < 0.001).