Regulation of early growth response-1 (Egr-1) gene expression by Stat1-independent type I interferon signaling and respiratory viruses
Abstract Respiratory virus infection is one of the leading causes of death in the world. Activation of the Jak-Stat pathway by Interferon-alpha/beta (IFN-α/β) in lung epithelial cells is critical for innate immunity to respiratory viruses. Transcriptional factor profiling in the transcriptome and RNA analysis revealed that Early growth response-1 (EGR1/Egr-1) was rapidly induced by IFN-α/β and Toll-like receptor (TLR) ligands in multiple cell types. Studies in mutant cell lines lacking components of the interferon-stimulated gene factor complex (ISGF-3) revealed that IFN-β induction of Egr-1 was independent of Stat1, Stat2, or Irf9. Activation of the Mek/Erk-1/2 pathway was implicated in the rapid induction of Egr-1 by IFN-β in serum-starved mouse lung epithelial cells. Interrogation of multiple microarray datasets revealed that respiratory viruses including coronaviruses induced IFN-β and regulated Egr-1 expression in human lung cell lines. Furthermore, bioinformatic analysis revealed that type I interferon-stimulated genes and Egr-1 inducible genes including transcription factors, mediators of cell growth, and chemokines were differentially regulated in the human lung cell lines after coronavirus infection, and in the lung biopsies of COVID-19 patients..
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2021 |
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Erschienen: |
2021 |
Enthalten in: |
Zur Gesamtaufnahme - volume:9 |
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Enthalten in: |
Computational and mathematical biophysics - 9(2021), 1 vom: 31. Dez., Seite 289-303 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Ramana, Chilakamarti V. [VerfasserIn] |
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Links: |
Volltext [kostenfrei] |
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Anmerkungen: |
© 2021 Chilakamarti V. Ramana et al., published by De Gruyter |
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doi: |
10.1515/cmb-2020-0129 |
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funding: |
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PPN (Katalog-ID): |
GRUY008823553 |
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520 | |a Abstract Respiratory virus infection is one of the leading causes of death in the world. Activation of the Jak-Stat pathway by Interferon-alpha/beta (IFN-α/β) in lung epithelial cells is critical for innate immunity to respiratory viruses. Transcriptional factor profiling in the transcriptome and RNA analysis revealed that Early growth response-1 (EGR1/Egr-1) was rapidly induced by IFN-α/β and Toll-like receptor (TLR) ligands in multiple cell types. Studies in mutant cell lines lacking components of the interferon-stimulated gene factor complex (ISGF-3) revealed that IFN-β induction of Egr-1 was independent of Stat1, Stat2, or Irf9. Activation of the Mek/Erk-1/2 pathway was implicated in the rapid induction of Egr-1 by IFN-β in serum-starved mouse lung epithelial cells. Interrogation of multiple microarray datasets revealed that respiratory viruses including coronaviruses induced IFN-β and regulated Egr-1 expression in human lung cell lines. Furthermore, bioinformatic analysis revealed that type I interferon-stimulated genes and Egr-1 inducible genes including transcription factors, mediators of cell growth, and chemokines were differentially regulated in the human lung cell lines after coronavirus infection, and in the lung biopsies of COVID-19 patients. | ||
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