| First Author | Chee LC | Year | 2013 |
| Journal | J Leukoc Biol | Volume | 93 |
| Issue | 2 | Pages | 235-43 |
| PubMed ID | 23136256 | Mgi Jnum | J:193750 |
| Mgi Id | MGI:5469519 | Doi | 10.1189/jlb.1211609 |
| Citation | Chee LC, et al. (2013) The granulocyte-colony stimulating factor receptor (G-CSFR) interacts with retinoic acid receptors (RARs) in the regulation of myeloid differentiation. J Leukoc Biol 93(2):235-43 |
| abstractText | The key roles of RARs and G-CSFR in the regulation of granulopoiesis have been well-documented. In this study, we sought to investigate the interaction between G-CSFR and RARs in myeloid differentiation of adult mice through conditional deletion of RARalpha or RARgamma on a G-CSFR(-/-) background and by pharmacological intervention of WT and G-CSFR(-/-) mice with a pan-RAR inverse agonist, NRX194310. Our findings show that residual granulopoiesis still persists in mice doubly null for G-CSFR and RARalpha or RARgamma, confirming that RARs and G-CSFR are dispensable in maintaining residual granulopoiesis. Moreover, an increase in mature myeloid cells was seen in the conditional RARgamma(Delta/Delta) mice and WT mice treated with NRX194310, likely mediated through increased G-CSF production. However, with the loss of G-CSFR, this expansion in granulopoiesis was attenuated, supporting the hypothesis that G-CSFR signaling interacts with RARs in the regulation of myeloid differentiation. |
