期刊
CELL REPORTS
卷 29, 期 4, 页码 860-+出版社
CELL PRESS
DOI: 10.1016/j.celrep.2019.09.035
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资金
- Plan Nacional de I+D+I 2013-2016 ISCIII (Institute of Health Carlos III) [PI16/01318, PI17/01244, PI17/0119, PI16/1900, PI19/00184]
- Gobierno del Principado de Asturias
- PCTI-Plan de Ciencia, Tecnologia e Innovacion 2013-2017 [IDI/2018/144]
- FEDER Funding Program of the European Union''
- Red Espan ola de Investigacion Renal (REDinREN) [RD16/0009/0020, RD016/0009/002, RD016/0009/001]
- Agencia Estatal de Investigacion (AEI) (ayuda Juan de la Cierva-Incorporacion) [IJCI-2017-33347]
- Instituto de Salud Carlos III (Contratos Sara Borrell) [CD16/00033]
- Severo Ochoa Excellence Accreditation [SEV-2016-0644]
In recent years, the macrophage colony-stimulating factor (M-CSF) and granulocyte-macrophage CSF (GM-CSF) cytokines have been identified as opposing regulators of the inflammatory program. However, the two cytokines are simultaneously present in the inflammatory milieu, and it is not clear how cells integrate these signals. In order to understand the regulatory networks associated with the GM/M-CSF signaling axis, we analyzed DNA methylation in human monocytes. Our results indicate that GM-CSF induces activation of the inflammatory program and extensive DNA methylation changes, while M-CSF-polarized cells are in a less differentiated state. This inflammatory program is mediated via JAK2 associated with the GM-CSF receptor and the downstream extracellular signal-regulated (ERK) signaling. However, PI3K signaling is associated with a negative regulatory loop of the inflammatory program and M-CSF autocrine signaling in GM-CSF-polarized monocytes. Our findings describe the regulatory networks associated with the GM/M-CSF signaling axis and how they contribute to the establishment of the inflammatory program associated with monocyte activation.
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