Glucocorticoid and cytokine crosstalk: Feedback, feedforward, and co-regulatory interactions determine repression or resistance.
| Autor: | Newton R; From the Airways Inflammation Research Group, Snyder Institute for Chronic Diseases, University of Calgary, Alberta T2N 4Z6, Canada, rnewton@ucalgary.ca., Shah S; the Arnie Charbonneau Cancer Institute, Department of Oncology, University of Calgary, Alberta T2N 4Z6, Canada., Altonsy MO; From the Airways Inflammation Research Group, Snyder Institute for Chronic Diseases, University of Calgary, Alberta T2N 4Z6, Canada.; the Faculty of Science, Sohag University, Sohag 82524, Egypt, and., Gerber AN; the Department of Medicine, National Jewish Health, Denver, Colorado 80206. |
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| Jazyk: | angličtina |
| Zdroj: | The Journal of biological chemistry [J Biol Chem] 2017 Apr 28; Vol. 292 (17), pp. 7163-7172. Date of Electronic Publication: 2017 Mar 10. |
| DOI: | 10.1074/jbc.R117.777318 |
| Abstrakt: | Inflammatory signals induce feedback and feedforward systems that provide temporal control. Although glucocorticoids can repress inflammatory gene expression, glucocorticoid receptor recruitment increases expression of negative feedback and feedforward regulators, including the phosphatase, DUSP1, the ubiquitin-modifying enzyme, TNFAIP3, or the mRNA-destabilizing protein, ZFP36. Moreover, glucocorticoid receptor cooperativity with factors, including nuclear factor-κB (NF-κB), may enhance regulator expression to promote repression. Conversely, MAPKs, which are inhibited by glucocorticoids, provide feedforward control to limit expression of the transcription factor IRF1, and the chemokine, CXCL10. We propose that modulation of feedback and feedforward control can determine repression or resistance of inflammatory gene expression toglucocorticoid. (© 2017 by The American Society for Biochemistry and Molecular Biology, Inc.) |
| Databáze: | MEDLINE |
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