Evidence map›Paper›PMID 27907187›Full record

ArticlePloS one2016

Substance P Induces HO-1 Expression in RAW 264.7 Cells Promoting Switch towards M2-Like Macrophages.

Giovanna Montana, Nadia Lampiasi

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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. TRPV1: The key bridge in neuroimmune interactions.Journal of intensive medicine · 2024
    Review
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  9. Cytotoxic and Anti-Inflammatory Triterpenoids in the Vines and Leaves ofInternational journal of molecular sciences · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Nucleic Acid-Based Dual Cross-Linked Hydrogels forACS applied materials & interfaces · 2019
    Article
  16. Anti-Aging Potential of Substance P-Based Hydrogel for Human Skin Longevity.International journal of molecular sciences · 2019
    Article
  17. Article
  18. Article
  19. Chemical Modulation ofACS central science · 2017
    Article
  20. Article
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

2 authors at 1 institution in 1 country.

Giovanna MontanaIstituto di Biomedicina e Immunologia Molecolare "Alberto Monroy", Consiglio Nazionale delle Ricerche, Via Ugo La Malfa, Palermo, Italy.
Nadia LampiasiIstituto di Biomedicina e Immunologia Molecolare "Alberto Monroy", Consiglio Nazionale delle Ricerche, Via Ugo La Malfa, Palermo, Italy.ORCID http://orcid.org/0000-0002-6831-4781
Istituto di Biomedicina e di Immunologia Molecolare Alberto Monroy · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Substance P (SP) is a neuropeptide that mediates many physiological as well as inflammatory responses. Recently, SP has been implicated in the resolution of inflammation through induction of M2 macrophages phenotype. The shift between M1-like and M2-like, allowing the resolution of inflammatory processes, also takes place by means of hemeoxygenase-1 (HO-1). HO-1 is induced in response to oxidative stress and inflammatory stimuli and modulates the immune response through macrophages polarisation. SP induces HO-1 expression in human periodontal ligament (PDL), the latter potentially plays a role in cytoprotection. We demonstrated that SP promotes M2-like phenotype from resting as well as from M1 macrophages. Indeed, SP triggers the production of interleukine-10 (IL-10), interleukine-4 (IL-4) and arginase-1 (Arg1) without nitric oxide (NO) generation. In addition, SP increases HO-1 expression in a dose- and time-dependent manner. Here we report that SP, without affecting cell viability, significantly reduces the production of pro-inflammatory cytokines and enzymes, such as tumor necrosis factor-alpha (TNF-α), interleukine-6 (IL-6), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), and ameliorates migration and phagocytic properties in LPS-stimulated RAW 264.7 cells. M2-like conversion required retention of NF-κB p65 into the cytoplasm and HO-1 induced expression. Silencing of the HO-1 mRNA expression reversed the induction of pro-inflammatory cytokines in RAW 264.7 stimulated by LPS and down-regulated anti-inflammatory hallmarks of M2 phenotype. In conclusion, our data show that SP treatment might be associated with anti-inflammatory effects in LPS-stimulated RAW 264.7 cells by suppressing NF-κB activation and inducing HO-1 expression.

Indexed as

AnimalsGene Expression RegulationHeme Oxygenase-1HumansInflammationInterleukin-10Interleukin-6LipopolysaccharidesMacrophagesMembrane ProteinsMiceNitric OxideNitric Oxide Synthase Type IIPeriodontal LigamentRAW 264.7 CellsSubstance PHeme Oxygenase-1Hmox1 protein, mouseInterleukin-10Interleukin-6interleukin-6, mouseLipopolysaccharidesMembrane ProteinsNitric OxideNitric Oxide Synthase Type IINos2 protein, mouseRela protein, mouseSubstance PTranscription Factor RelATumor Necrosis Factor-alpha

Identifiers

PMID27907187
PMCPMC5132328
OpenAlexW2557352986

What OpenQuestion holds

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LicenceCC BY
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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.