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Bolívar S, Anfossi R, Humeres C, et al. IFN-β Plays Both Pro- and Anti-inflammatory Roles in the Rat Cardiac Fibroblast Through Differential STAT Protein Activation. Front Pharmacol. 2018;9:1368doi: 10.3389/fphar.2018.01368.
Bolívar, S., Anfossi, R., Humeres, C., Vivar, R., Boza, P., Muñoz, C., Pardo-Jimenez, V., Olivares-Silva, F., & Díaz-Araya, G. (2018). IFN-β Plays Both Pro- and Anti-inflammatory Roles in the Rat Cardiac Fibroblast Through Differential STAT Protein Activation. Frontiers in pharmacology, 91368. https://doi.org/10.3389/fphar.2018.01368
Bolívar, Samir, et al. "IFN-β Plays Both Pro- and Anti-inflammatory Roles in the Rat Cardiac Fibroblast Through Differential STAT Protein Activation." Frontiers in pharmacology vol. 9 (2018): 1368. doi: https://doi.org/10.3389/fphar.2018.01368
Bolívar S, Anfossi R, Humeres C, Vivar R, Boza P, Muñoz C, Pardo-Jimenez V, Olivares-Silva F, Díaz-Araya G. IFN-β Plays Both Pro- and Anti-inflammatory Roles in the Rat Cardiac Fibroblast Through Differential STAT Protein Activation. Front Pharmacol. 2018 Nov 28;9:1368. doi: 10.3389/fphar.2018.01368. eCollection 2018. PMID: 30555324; PMCID: PMC6280699.
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Front Pharmacol. 2018 Nov 28;9:1368. doi: 10.3389/fphar.2018.01368. eCollection 2018.

IFN-β Plays Both Pro- and Anti-inflammatory Roles in the Rat Cardiac Fibroblast Through Differential STAT Protein Activation.

Frontiers in pharmacology

Samir Bolívar, Renatto Anfossi, Claudio Humeres, Raúl Vivar, Pía Boza, Claudia Muñoz, Viviana Pardo-Jimenez, Francisco Olivares-Silva, Guillermo Díaz-Araya

Affiliations

  1. Faculty of Chemistry and Pharmacy, Atlantic University, Barranquilla, Colombia.
  2. Department of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santiago, Chile.
  3. Advanced Center for Chronic Diseases, Faculty of Chemical and Pharmaceutical Sciences and Faculty of Medicine, University of Chile, Santiago, Chile.

PMID: 30555324 PMCID: PMC6280699 DOI: 10.3389/fphar.2018.01368

Abstract

Cardiac fibroblasts (CFs) contribute to theinflammatory response to tissue damage, secreting both pro- and anti-inflammatory cytokines and chemokines. Interferon beta (IFN-β) induces the phosphorylation of signal transducer and activator of transcription (STAT) proteins through the activation of its own receptor, modulating the secretion of cytokines and chemokines which regulate inflammation. However, the role of IFN-β and STAT proteins in modulating the inflammatory response of CF remains unknown. CF were isolated from adult male rats and subsequently stimulated with IFN-β to evaluate the participation of STAT proteins in secreting chemokines, cytokines, cell adhesion proteins expression and in their capacity to recruit neutrophils. In addition, in CF in which the TRL4 receptor was pre-activated, the effect of INF-β on the aforementioned responses was also evaluated. Cardiac fibroblasts stimulation with IFN-β showed an increase in STAT1, STAT2, and STAT3 phosphorylation. IFN-β stimulation through STAT1 activation increased proinflammatory chemokines MCP-1 and IP-10 secretion, whereas IFN-β induced activation of STAT3 increased cytokine secretion of anti-inflammatory IL-10. Moreover, in TLR4-activated CF, IFN-β through STAT2 and/or STAT3, produced an anti-inflammatory effect, reducing pro-IL-1β, TNF-α, IL-6, MCP-1, and IP-10 secretion; and decreasing neutrophil recruitment by decreasing ICAM-1 and VCAM-1 expression. Altogether, our results indicate that IFN-β exerts both pro-inflammatory and anti-inflammatory effects in non-stimulated CF, through differential activation of STAT proteins. When CF were previously treated with an inflammatory agent such as TLR-4 activation, IFN-β effects were predominantly anti-inflammatory.

Keywords: IFN-β (interferon β); STAT; anti-infammatory; cardiac fibroblast; proinflammatory

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