Evidence map›Paper›PMID 33459958›Full record

ArticleMolecular biology reports2021

Resolvin D1 and E1 promote resolution of inflammation in rat cardiac fibroblast in vitro.

Aimeé Salas-Hernández, Claudio Espinoza-Pérez, Raúl Vivar, Jenaro Espitia-Corredor, José Lillo, Pablo Parra-Flores, Carlos F Sánchez-Ferrer, Concepción Peiró, Guillermo Díaz-Araya

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Article in Molecular biology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 25 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 4 institutions in 3 countries.

Aimeé Salas-HernándezDepartment of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santos Dumont 964, Independencia, Santiago, Chile.
Claudio Espinoza-PérezDepartment of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santos Dumont 964, Independencia, Santiago, Chile.
Raúl VivarPharmacology Program, Biomedical Sciences Institute, University of Chile, Independencia 1027, Independencia, Santiago, Chile.
Jenaro Espitia-CorredorDepartment of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santos Dumont 964, Independencia, Santiago, Chile.
José LilloDepartment of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santos Dumont 964, Independencia, Santiago, Chile.
Pablo Parra-FloresDepartment of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santos Dumont 964, Independencia, Santiago, Chile.
Carlos F Sánchez-FerrerDepartment of Pharmacology, Faculty of Medicine, Universidad Autónoma de Madrid and Instituto de Investigación Sanitaria Hospital Universitario La Paz (IdiPAZ), Madrid, Spain.
Concepción PeiróDepartment of Pharmacology, Faculty of Medicine, Universidad Autónoma de Madrid and Instituto de Investigación Sanitaria Hospital Universitario La Paz (IdiPAZ), Madrid, Spain.
Guillermo Díaz-ArayaDepartment of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santos Dumont 964, Independencia, Santiago, Chile. gadiaz@ciq.uchile.cl.ORCID http://orcid.org/0000-0001-7960-8104
University of Chile · CLHospital Universitario La Paz · ESAdvanced Center for Chronic Diseases · CLUniversidad de Costa Rica · CR

Funding

fondecyt 1170425Universidad de Costa Rica OAICE-CAB-03-031-2015
6 · The paper itself

Abstract

Cardiac fibroblasts (CFs) have a key role in the inflammatory response after cardiac injury and are necessary for wound healing. Resolvins are potent agonists that control the duration and magnitude of inflammation. They decrease mediators of pro-inflammatory expression, reduce neutrophil migration to inflammation sites, promote the removal of microbes and apoptotic cells, and reduce exudate. However, whether resolvins can prevent pro-inflammatory-dependent effects in CFs is unknown. Thus, the present work was addressed to study whether resolvin D1 and E1 (RvD1 and RvE1) can prevent pro-inflammatory effects on CFs after lipopolysaccharide (LPS) challenge. For this, CFs were stimulated with LPS, in the presence or absence of RvD1 or RvE1, to analyze its effects on intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion protein 1 (VCAM-1), monocyte adhesion and the cytokine levels of tumor necrosis factor alpha (TNF-α), interleukin-6(IL-6), interleukin-1beta (IL-1β), monocyte chemoattractant protein-1 (MCP-1) and interleukin-10 (IL-10). Our results showed that CFs are expressing ALX/FPR2 and ChemR23, RvD1 and RvE1 receptors, respectively. RvD1 and RvE1 prevent the increase of ICAM-1 and VCAM-1 protein levels and the adhesion of spleen mononuclear cells to CFs induced by LPS. Finally, RvD1, but not RvE1, prevents the LPS-induced increase of IL-6, MCP-1, TNF-α, and IL-10. In conclusion, our findings provide evidence that in CFs, RvD1 and RvE1 might actively participate in the prevention of inflammatory response triggered by LPS.

Indexed as

AnimalsCell MovementCytokinesDocosahexaenoic AcidsEicosapentaenoic AcidFibroblastsGene Expression RegulationHeart InjuriesHumansInflammationInterleukin-1betaLipopolysaccharidesNeutrophilsRatsTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-15S,12R,18R-trihydroxy-6Z,8E,10E,14Z,16E-eicosapentaenoic acidCytokinesDocosahexaenoic AcidsEicosapentaenoic AcidIL1B protein, humanInterleukin-1betaLipopolysaccharidesresolvin D1Tumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1Cardiac fibroblastsCytokinesResolvin D1Resolvin E1

Identifiers

PMID33459958
OpenAlexW3123514482

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.