Evidence map›Paper›PMID 34204273›Full record

ArticleCells2021

The N-Formyl Peptide Receptor 2 (FPR2) Agonist MR-39 Exhibits Anti-Inflammatory Activity in LPS-Stimulated Organotypic Hippocampal Cultures.

Ewa Trojan, Kinga Tylek, Monika Leśkiewicz, Władysław Lasoń, Lars-Ove Brandenburg, Marcello Leopoldo, Enza Lacivita, Agnieszka Basta-Kaim

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

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  11. Paclitaxel triggers molecular and cellular changes in the choroid plexus.Frontiers in pain research (Lausanne, Switzerland) · 2024
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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

8 authors at 3 institutions in 3 countries.

Ewa TrojanLaboratory of Immunoendocrinology, Department of Experimental Neuroendocrinology, Maj Institute of Pharmacology Polish Academy of Sciences, 12 Smętna Str., 31-343 Kraków, Poland.ORCID 0000-0002-9573-7026
Kinga TylekLaboratory of Immunoendocrinology, Department of Experimental Neuroendocrinology, Maj Institute of Pharmacology Polish Academy of Sciences, 12 Smętna Str., 31-343 Kraków, Poland.
Monika LeśkiewiczLaboratory of Immunoendocrinology, Department of Experimental Neuroendocrinology, Maj Institute of Pharmacology Polish Academy of Sciences, 12 Smętna Str., 31-343 Kraków, Poland.
Władysław LasońLaboratory of Immunoendocrinology, Department of Experimental Neuroendocrinology, Maj Institute of Pharmacology Polish Academy of Sciences, 12 Smętna Str., 31-343 Kraków, Poland.
Lars-Ove BrandenburgInstitute of Anatomy, Rostock University Medical Center, 18057 Rostock, Germany.ORCID 0000-0002-6126-8153
Marcello LeopoldoDepartment of Pharmacy-Drug Sciences, University of Bari, Via Orabona 4, 70125 Bari, Italy.
Enza LacivitaDepartment of Pharmacy-Drug Sciences, University of Bari, Via Orabona 4, 70125 Bari, Italy.ORCID 0000-0003-2443-1174
Agnieszka Basta-KaimLaboratory of Immunoendocrinology, Department of Experimental Neuroendocrinology, Maj Institute of Pharmacology Polish Academy of Sciences, 12 Smętna Str., 31-343 Kraków, Poland.ORCID 0000-0002-3109-0040
Maj Institute of Pharmacology · PLUniversity of Bari Aldo Moro · ITUniversity of Rostock · DE

Funding

Alzheimer's Association AARG-NTF-18-565227Narodowe Centrum Nauki 2017/26/M/NZ7/01048 (HARMONIA)
6 · The paper itself

Abstract

Accumulating evidence indicates a pivotal role for chronic inflammatory processes in the pathogenesis of neurodegenerative and psychiatric disorders. G protein-coupled formyl peptide receptor 2 (FPR2) mediates pro-inflammatory or anti-/pro-resolving effects upon stimulation with biased agonists. We aimed to evaluate the effects of a new FPR2 ureidopropanamide agonist, compound MR-39, on neuroinflammatory processes in organotypic hippocampal cultures (OHCs) derived from control (WT) and knockout FPR2-/- mice (KO) exposed to bacterial endotoxin (lipopolysaccharide; LPS). Higher LPS-induced cytokine expression and basal release were observed in KO FPR2 cultures than in WT cultures, suggesting that a lack of FPR2 enhances the OHCs response to inflammatory stimuli. Pretreatment with MR-39 abolished some of the LPS-induced changes in the expression of genes related to the M1/M2 phenotypes (including

Indexed as

AnimalsAnti-Inflammatory AgentsCytokinesHippocampusInflammasomesInflammationLipopolysaccharidesMiceMice, KnockoutOrgan Culture TechniquesReceptors, Formyl PeptideAnti-Inflammatory AgentsCytokinesformyl peptide receptor 2, mouseInflammasomesLipopolysaccharidesReceptors, Formyl Peptideformyl peptide receptor 2hippocampal organotypic cultureslipopolysaccharideMR-39NLPR3 inflammasome

Identifiers

PMID34204273
PMCPMC8235773
OpenAlexW3167037214

What OpenQuestion holds

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LicenceCC BY
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.