p38δ controls Mitogen- and Stress-activated Kinase-1 (MSK1) function in response to toll-like receptor activation in macrophages.

Autor:	Díaz-Mora E; Department of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC (CNB-CSIC), Madrid, Spain., González-Romero D; Department of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC (CNB-CSIC), Madrid, Spain., Meireles-da-Silva M; Department of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC (CNB-CSIC), Madrid, Spain., Sanz-Ezquerro JJ; Department of Molecular and Cellular Biology, Centro Nacional de Biotecnología/CSIC (CNB-CSIC), Madrid, Spain., Cuenda A; Department of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC (CNB-CSIC), Madrid, Spain.
Jazyk:	angličtina
Zdroj:	Frontiers in cell and developmental biology [Front Cell Dev Biol] 2023 Feb 09; Vol. 11, pp. 1083033. Date of Electronic Publication: 2023 Feb 09 (Print Publication: 2023).
DOI:	10.3389/fcell.2023.1083033
Abstrakt:	Mitogen- and Stress-activated Kinase (MSK) 1 is a nuclear protein, activated by p38α Mitogen-Activated Kinase (MAPK) and extracellular signal-regulated kinase (ERK1/2), that modulate the production of certain cytokines in macrophages. Using knockout cells and specific kinase inhibitors, we show that, besides p38α and ERK1/2, another p38MAPK, p38δ, mediates MSK phosphorylation and activation, in LPS-stimulated macrophages. Additionally, recombinant MSK1 was phosphorylated and activated by recombinant p38δ, to the same extent than by p38α, in in vitro experiments. Moreover, the phosphorylation of the transcription factors CREB and ATF1, that are MSK physiological substrates, and the expression of the CREB-dependent gene encoding DUSP1, were impaired in p38δ-deficient macrophages. Also, the transcription of IL-1Ra mRNA, that is MSK-dependent, was reduced. Our results indicate that MSK activation can be one possible mechanism by which p38δ regulates the production of a variety of inflammatory molecules involved in immune innate response. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The handling editor PAL declared a shared affiliation with the author(s) AC, EDM, MMS, DGR, JJSE at the time of review. (Copyright © 2023 Díaz-Mora, González-Romero, Meireles-da-Silva, Sanz-Ezquerro and Cuenda.)
Databáze:	MEDLINE
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