Evidence map›Paper›PMID 27752805›Full record

ArticleMolecular and cellular biochemistry2017

Methionine and methionine sulfoxide treatment induces M1/classical macrophage polarization and modulates oxidative stress and purinergic signaling parameters.

Lien M Dos Santos, Tatiane M da Silva, Juliana H Azambuja, Priscila T Ramos, Pathise S Oliveira, Elita F da Silveira, Nathalia S Pedra, Kennia Galdino, Carlus A T do Couto, Mayara S P Soares and 4 more

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 49 citations in OpenAlex.

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  13. The significant role of amino acid metabolic reprogramming in cancer.Cell communication and signaling : CCS · 2024
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  19. Clinical development of metabolic inhibitors for oncology.The Journal of clinical investigation · 2022
    Review
  20. Review
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

14 authors at 3 institutions in 1 country.

Lien M Dos SantosLaboratório de Neuroquímica, Inflamação e Câncer, Centro de Ciências Químicas Farmacêuticas e de Alimentos, Universidade Federal de Pelotas (UFPel), Pelotas, RS, Brazil.
Tatiane M da SilvaLaboratório de Biomarcadores, Centro de Ciências Químicas Farmacêuticas e de Alimentos, Universidade Federal de Pelotas (UFPel), Campus Universitário s/n, Capão do Leão, Pelotas, RS, 96160-000, Brazil.
Juliana H AzambujaLaboratório de Neuroquímica, Inflamação e Câncer, Centro de Ciências Químicas Farmacêuticas e de Alimentos, Universidade Federal de Pelotas (UFPel), Pelotas, RS, Brazil.
Priscila T RamosLaboratório de Neuroquímica, Inflamação e Câncer, Centro de Ciências Químicas Farmacêuticas e de Alimentos, Universidade Federal de Pelotas (UFPel), Pelotas, RS, Brazil.
Pathise S OliveiraLaboratório de Biomarcadores, Centro de Ciências Químicas Farmacêuticas e de Alimentos, Universidade Federal de Pelotas (UFPel), Campus Universitário s/n, Capão do Leão, Pelotas, RS, 96160-000, Brazil.
Elita F da SilveiraDepartamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Rio Grande (FURG), Rio Grande, RS, Brazil.
Nathalia S PedraLaboratório de Neuroquímica, Inflamação e Câncer, Centro de Ciências Químicas Farmacêuticas e de Alimentos, Universidade Federal de Pelotas (UFPel), Pelotas, RS, Brazil.
Kennia GaldinoLaboratório de Neuroquímica, Inflamação e Câncer, Centro de Ciências Químicas Farmacêuticas e de Alimentos, Universidade Federal de Pelotas (UFPel), Pelotas, RS, Brazil.
Carlus A T do CoutoLaboratório de Neuroquímica, Inflamação e Câncer, Centro de Ciências Químicas Farmacêuticas e de Alimentos, Universidade Federal de Pelotas (UFPel), Pelotas, RS, Brazil.
Mayara S P SoaresLaboratório de Neuroquímica, Inflamação e Câncer, Centro de Ciências Químicas Farmacêuticas e de Alimentos, Universidade Federal de Pelotas (UFPel), Pelotas, RS, Brazil.
Rejane G TavaresLaboratório de Biomarcadores, Centro de Ciências Químicas Farmacêuticas e de Alimentos, Universidade Federal de Pelotas (UFPel), Campus Universitário s/n, Capão do Leão, Pelotas, RS, 96160-000, Brazil.
Roselia M SpanevelloLaboratório de Neuroquímica, Inflamação e Câncer, Centro de Ciências Químicas Farmacêuticas e de Alimentos, Universidade Federal de Pelotas (UFPel), Pelotas, RS, Brazil.
Francieli M StefanelloLaboratório de Biomarcadores, Centro de Ciências Químicas Farmacêuticas e de Alimentos, Universidade Federal de Pelotas (UFPel), Campus Universitário s/n, Capão do Leão, Pelotas, RS, 96160-000, Brazil. fmstefanello@gmail.com.
Elizandra BraganholDepartamento de Ciências Básicas da Saúde, Universidade Federal de Ciências da Saúde de Porto Alegre (UFCSPA), Rua Sarmento Leite, 245 - Anexo I - sala 303, Porto Alegre, RS, 90050-170, Brazil. ebraganhol@ufcspa.edu.br.
Universidade Federal de Pelotas · BRUniversidade Federal de Ciências da Saúde de Porto Alegre · BRUniversidade Federal do Rio Grande · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Methionine is an essential amino acid involved in critical metabolic process, and regulation of methionine flux through metabolism is important to supply this amino acid for cell needs. Elevation in plasma methionine commonly occurs due to mutations in methionine-metabolizing enzymes, such as methionine adenosyltransferase. Hypermethioninemic patients exhibit clinical manifestations, including neuronal and liver disorders involving inflammation and tissue injury, which pathophysiology is not completely established. Here, we hypothesize that alterations in macrophage inflammatory response may contribute to deleterious effects of hypermethioninemia. To this end, macrophage primary cultures were exposed to methionine (1 mM) and/or its metabolite methionine sulfoxide (0.5 mM), and M1/proinflammatory or M2/anti-inflammatory macrophage polarization was evaluated. In addition, inflammation-related pathways including oxidative stress parameters, as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities; reactive oxygen species (ROS) production, and purinergic signaling, as ATP/ADP/AMPase activities, were investigated. Methionine and/or methionine sulfoxide induced M1/classical macrophage activation, which is related to proinflammatory responses characterized by increased iNOS activity and TNF-α release. Further experiments showed that treatments promoted alterations on redox state of macrophages by differentially modulated SOD and CAT activities and ROS levels. Finally, methionine and/or methionine sulfoxide treatment also altered the extracellular nucleotide metabolism, promoting an increase of ATPase/ADPase activities in macrophages. In conclusion, these findings contribute to better understand the participation of proinflammatory responses in cell injury observed in hypermethioninemic patients.

Indexed as

AnimalsCatalaseGlutathione PeroxidaseMacrophagesMaleMethionineMiceOxidative StressReactive Oxygen SpeciesSignal TransductionSuperoxide DismutaseCatalaseGlutathione PeroxidaseMethioninemethionine sulfoxideReactive Oxygen SpeciesSuperoxide DismutaseEctonucleotidasesMacrophage polarizationMethionineMethionine sulfoxideOxidative stress

Identifiers

PMID27752805
OpenAlexW2537356793

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.