Evidence map›Paper›PMID 27359332›Full record

ArticlePloS one2016

[Nle4, D-Phe7]-α-MSH Inhibits Toll-Like Receptor (TLR)2- and TLR4-Induced Microglial Activation and Promotes a M2-Like Phenotype.

Lila Carniglia, Delia Ramírez, Daniela Durand, Julieta Saba, Carla Caruso, Mercedes Lasaga

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Acute impact of afamelanotide on UVR erythemal and melanogenic responses in healthy humans in vivo: an exploratory study.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026
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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

6 authors at 2 institutions in 1 country.

Lila CarnigliaInstitute of Biomedical Research (INBIOMED -UBA- CONICET), School of Medicine, University of Buenos Aires, Buenos Aires, 1121, Argentina.
Delia RamírezInstitute of Biomedical Research (INBIOMED -UBA- CONICET), School of Medicine, University of Buenos Aires, Buenos Aires, 1121, Argentina.
Daniela DurandInstitute of Biomedical Research (INBIOMED -UBA- CONICET), School of Medicine, University of Buenos Aires, Buenos Aires, 1121, Argentina.
Julieta SabaInstitute of Biomedical Research (INBIOMED -UBA- CONICET), School of Medicine, University of Buenos Aires, Buenos Aires, 1121, Argentina.
Carla CarusoInstitute of Biomedical Research (INBIOMED -UBA- CONICET), School of Medicine, University of Buenos Aires, Buenos Aires, 1121, Argentina.
Mercedes LasagaInstitute of Biomedical Research (INBIOMED -UBA- CONICET), School of Medicine, University of Buenos Aires, Buenos Aires, 1121, Argentina.
Consejo Nacional de Investigaciones Científicas y Técnicas · ARUniversity of Buenos Aires · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

α-melanocyte stimulating hormone (α-MSH) is an anti-inflammatory peptide, proved to be beneficial in many neuroinflammatory disorders acting through melanocortin receptor 4 (MC4R). We previously determined that rat microglial cells express MC4R and that NDP-MSH, an analog of α-MSH, induces PPAR-γ expression and IL-10 release in these cells. Given the great importance of modulation of glial activation in neuroinflammatory disorders, we tested the ability of NDP-MSH to shape microglial phenotype and to modulate Toll-like receptor (TLR)-mediated inflammatory responses. Primary rat cultured microglia were stimulated with NDP-MSH followed by the TLR2 agonist Pam3CSK4 or the TLR4 agonist LPS. NDP-MSH alone induced expression of the M2a/M2c marker Ag1 and reduced expression of the M2b marker Il-4rα and of the LPS receptor Tlr4. Nuclear translocation of NF-κB subunits p65 and c-Rel was induced by LPS and these effects were partially prevented by NDP-MSH. NDP-MSH reduced LPS- and Pam3CSK4-induced TNF-α release but did not affect TLR-induced IL-10 release. Also, NDP-MSH inhibited TLR2-induced HMGB1 translocation from nucleus to cytoplasm and TLR2-induced phagocytic activity. Our data show that NDP-MSH inhibits TLR2- and TLR4-mediated proinflammatory mechanisms and promotes microglial M2-like polarization, supporting melanocortins as useful tools for shaping microglial activation towards an alternative immunomodulatory phenotype.

Indexed as

alpha-MSHAnimalsCells, CulturedInterleukin-10LipopeptidesLipopolysaccharidesMicrogliaRatsToll-Like Receptor 2Toll-Like Receptor 4Tumor Necrosis Factor-alphaalpha-MSHInterleukin-10LipopeptidesLipopolysaccharidesMSH, 4-Nle-7-Phe-alpha-Pam(3)CSK(4) peptideToll-Like Receptor 2Toll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID27359332
PMCPMC4928783
OpenAlexW2470993797

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.