Evidence map›Paper›PMID 31391499›Full record

ArticleScientific reports2019

High Glucose Environments Interfere with Bone Marrow-Derived Macrophage Inflammatory Mediator Release, the TLR4 Pathway and Glucose Metabolism.

Thais Soprani Ayala, Fernando Henrique Galvão Tessaro, Grasielle Pereira Jannuzzi, Leonardo Mendes Bella, Karen Spadari Ferreira, Joilson O Martins

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

39 citing papers in PubMed, 68 citations in OpenAlex.

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  16. Novel Insights into Sporotrichosis and Diabetes.Journal of fungi (Basel, Switzerland) · 2024
    Review
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  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

6 authors at 2 institutions in 1 country.

Thais Soprani AyalaLaboratory of Immunoendocrinology, Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences of University Sao Paulo (FCF/USP), São Paulo, Brazil.
Fernando Henrique Galvão TessaroLaboratory of Immunoendocrinology, Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences of University Sao Paulo (FCF/USP), São Paulo, Brazil.ORCID http://orcid.org/0000-0002-0389-5976
Grasielle Pereira JannuzziLaboratory of Cellular Immunology and Biochemistry of Fungus and Protozoa, Department of Pharmaceutical Sciences Analysis, Federal University of São Paulo, São Paulo, Brazil.
Leonardo Mendes BellaLaboratory of Immunoendocrinology, Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences of University Sao Paulo (FCF/USP), São Paulo, Brazil.
Karen Spadari FerreiraLaboratory of Cellular Immunology and Biochemistry of Fungus and Protozoa, Department of Pharmaceutical Sciences Analysis, Federal University of São Paulo, São Paulo, Brazil.
Joilson O MartinsLaboratory of Immunoendocrinology, Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences of University Sao Paulo (FCF/USP), São Paulo, Brazil. martinsj@usp.br.ORCID http://orcid.org/0000-0003-2630-7038
Universidade de São Paulo · BRUniversidade Federal de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages may be a crucial aspect of diabetic complications associated with the inflammatory response. In this study, we examined how hyperglycaemia, a common aspect of diabetes, modulates bone marrow-derived macrophages (BMDMs) under an inflammatory stimulus. To perform this study, BMDMs from non-diabetic and diabetic (60 mg/kg alloxan, i.v.) male C57BL/6 mice (CEUA/FCF/USP-488) were cultured under normal (5.5 mM) and high glucose (HG, 25 or 40 mM) conditions and stimulated or not stimulated with lipopolysaccharide (LPS, 100 ng/mL). Compared to the BMDMs from the normoglycaemic mice, the LPS-stimulated BMDMs from the diabetic mice presented reduced TLR4 expression on the cell surface, lower phagocytic capacity, and reduced secretion of NO and lactate but greater oxygen consumption and greater phosphorylation of p46 SAPK/JNK, p42 ERK MAPK, pAKT and pPKC-δ. When the BMDMs from the non-diabetic mice were cultured under high-glucose conditions and stimulated with LPS, TLR4 expression was reduced on the cell surface and NO and H

Indexed as

AlloxanAnimalsBlood GlucoseCells, CulturedCulture MediaDiabetes Mellitus, ExperimentalHumansInflammation MediatorsLipopolysaccharidesMacrophagesMaleMicePrimary Cell CultureSignal TransductionToll-Like Receptor 4AlloxanBlood GlucoseCulture MediaInflammation MediatorsLipopolysaccharidesTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID31391499
PMCPMC6686006
OpenAlexW2966356915

What OpenQuestion holds

Textmetadata
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.