Evidence map›Paper›PMID 24078776›Full record

ArticleMediators of inflammation2013

SOCS3 expression correlates with severity of inflammation, expression of proinflammatory cytokines, and activation of STAT3 and p38 MAPK in LPS-induced inflammation in vivo.

João Antônio Chaves de Souza, Andressa Vilas Boas Nogueira, Pedro Paulo Chaves de Souza, Yeon Jung Kim, Caroline Silva Lobo, Guilherme José Pimentel Lopes de Oliveira, Joni Augusto Cirelli, Gustavo Pompermaier Garlet, Carlos Rossa

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
2.8field-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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.

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  15. SOCS2 regulates alveolar bone loss in Aggregatibacter actinomycetemcomitans-induced periodontal disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
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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

9 authors at 3 institutions in 1 country.

João Antônio Chaves de SouzaDepartment of Diagnosis and Surgery, School of Dentistry at Araraquara, Universidade Estadual Paulista, Rua Humaitá, 1680-Centro, 14801-903 Araraquara, SP, Brazil.
Andressa Vilas Boas Nogueira
Pedro Paulo Chaves de Souza
Yeon Jung Kim
Caroline Silva Lobo
Guilherme José Pimentel Lopes de Oliveira
Joni Augusto Cirelli
Gustavo Pompermaier Garlet
Carlos Rossa
Universidade Estadual Paulista (Unesp) · BRUniversidade de Santo Amaro · BRUniversidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SOCS3 is an inducible endogenous negative regulator of JAK/STAT pathway, which is relevant in inflammatory conditions. We used a model of LPS-induced periodontal disease in rats to correlate SOCS3 expression with the inflammatory status. In vitro we used a murine macrophage cell line to assess the physical interaction between SOCS3 and STAT3 by coimmunoprecipitation. 30 ug of LPS from Escherichia coli were injected in the gingival tissues on the palatal aspect of first molars of the animals 3x/week for up to 4 weeks. Control animals were injected with the vehicle (PBS). The rats were sacrificed at 7, 15, and 30 days. Inflammation and gene expression were assessed by stereometric analysis, immunohistochemistry, RT-qPCR, and western blot. LPS injections increased inflammation, paralleled by an upregulation of SOCS3, of the proinflammatory cytokines IL-1 β , IL-6, and TNF- α and increased phosphorylation of STAT3 and p38 MAPK. SOCS3 expression accompanied the severity of inflammation and the expression of proinflammatory cytokines, as well as the activation status of STAT3 and p38 MAPK. LPS stimulation in a macrophage cell line in vitro induced transient STAT3 activation, which was inversely correlated with a dynamic physical interaction with SOCS3, suggesting that this may be a mechanism for SOCS3 regulatory function.

Indexed as

Gene Expression RegulationAnimalsCell LineCytokinesEnzyme ActivationImmunohistochemistryInflammationLipopolysaccharidesMacrophagesMaleMicep38 Mitogen-Activated Protein KinasesPhosphorylationRatsRats, WistarReal-Time Polymerase Chain ReactionCytokinesLipopolysaccharidesp38 Mitogen-Activated Protein KinasesSocs3 protein, mouseSocs3 protein, ratSTAT3 Transcription FactorSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling Proteins

Identifiers

PMID24078776
PMCPMC3775441
OpenAlexW1986116779

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.