| First Author | Lee GT | Year | 2011 |
| Journal | Mol Immunol | Volume | 48 |
| Issue | 12-13 | Pages | 1540-7 |
| PubMed ID | 21571370 | Mgi Jnum | J:172437 |
| Mgi Id | MGI:5007840 | Doi | 10.1016/j.molimm.2011.04.019 |
| Citation | Lee GT, et al. (2011) Bone morphogenetic protein 6-induced interleukin-1beta expression in macrophages requires PU.1/Smad1 interaction. Mol Immunol 48(12-13):1540-7 |
| abstractText | Interleukin 1beta (IL-1beta) is a pro-inflammatory cytokine secreted by activated macrophages and monocytes. Previously, we have reported that bone morphogenetic protein-6 (BMP-6) induces inducible nitric oxide synthase (iNOS) expression via IL-1beta in macrophages. In the present study, we demonstrate that BMP-6 increases IL-1beta expression in macrophages via the receptors ALK3 and BMPRII as well as the downstream signaling protein Smad1. Surprisingly though, inhibition of the ERK and JNK non-Smad pathways also completely blocked the induction of IL-1beta by BMP-6 in macrophages. Further analysis revealed that a physical interaction between the transcription factor PU.1 and Smad 1 is necessary for the upregulation of IL-1beta expression by BMP-6 in macrophages. Taken together, these results demonstrate that BMP-6-induced IL-1beta expression in macrophages is mediated via a cross-talk between the Smad and the non-Smad pathways through Smad1 and PU.1. |
