Evidence map›Paper›PMID 30555324›Full record

ArticleFrontiers in pharmacology2018

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

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

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 2 pooled it
1.6field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

51 citing papers in PubMed, 2 syntheses or guidelines pooled it, 73 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 1 institution in 2 countries.

Samir BolívarFaculty of Chemistry and Pharmacy, Atlantic University, Barranquilla, Colombia.
Renatto AnfossiDepartment of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santiago, Chile.
Claudio HumeresDepartment of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santiago, Chile.
Raúl VivarDepartment of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santiago, Chile.
Pía BozaDepartment of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santiago, Chile.
Claudia MuñozDepartment of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santiago, Chile.
Viviana Pardo-JimenezDepartment of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santiago, Chile.
Francisco Olivares-SilvaDepartment of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santiago, Chile.
Guillermo Díaz-ArayaDepartment of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santiago, Chile.
University of Chile · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

anti-infammatorycardiac fibroblastIFN-β (interferon β)proinflammatorySTAT

Identifiers

PMID30555324
PMCPMC6280699
OpenAlexW2902807143

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.