AI Article Synopsis
- Interleukin 1β (IL-1β) is a cytokine involved in inflammation, produced by activated macrophages and monocytes.
- Bone morphogenetic protein-6 (BMP-6) plays a role in increasing IL-1β expression, utilizing specific receptors (ALK3, BMPRII) and the signaling protein Smad1 in macrophages.
- The study uncovers that both Smad and non-Smad pathways need to interact for IL-1β upregulation, highlighting the importance of the transcription factor PU.1 in this process.
Article Abstract
Interleukin 1β (IL-1β) 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-1β in macrophages. In the present study, we demonstrate that BMP-6 increases IL-1β 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-1β 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-1β expression by BMP-6 in macrophages. Taken together, these results demonstrate that BMP-6-induced IL-1β expression in macrophages is mediated via a cross-talk between the Smad and the non-Smad pathways through Smad1 and PU.1.
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| http://dx.doi.org/10.1016/j.molimm.2011.04.019 | DOI Listing |
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