Evidence map›Paper›PMID 23731754›Full record

ArticleJournal of inflammation (London, England)2013

Lipopolysaccharide induces the expression of an autocrine prolactin loop enhancing inflammatory response in monocytes.

Gonzalo López-Rincón, Ana L Pereira-Suárez, Susana Del Toro-Arreola, Pedro E Sánchez-Hernández, Alejandra Ochoa-Zarzosa, José Francisco Muñoz-Valle, Ciro Estrada-Chávez

Open access · goldAbstract read
In one paragraph

Article in Journal of inflammation (London, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 33 citations in OpenAlex.

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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

7 authors at 4 institutions in 2 countries.

Gonzalo López-RincónUnidad de Biotecnología Médica y Farmacéutica, Centro de Investigación y Asistencia en Tecnología y Diseño del Estado de Jalisco A,C, Guadalajara, Jalisco 44270, México. cestrada.ciatej@gmail.com.
Ana L Pereira-Suárez
Susana Del Toro-Arreola
Pedro E Sánchez-Hernández
Alejandra Ochoa-Zarzosa
José Francisco Muñoz-Valle
Ciro Estrada-Chávez
Universidad de Guadalajara · MXCentro de Investigación y Asistencia en Tecnología y Diseño del Estado de JaliscoSecretaría de Salud de Jalisco · MXUniversidad Michoacana de San Nicolás de Hidalgo · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProlactin from pituitary gland helps maintain homeostasis but it is also released in immune cells where its function is not completely understood. Pleiotropic functions of prolactin (PRL) might be mediated by different isoforms of its receptor (PRLr).

methodsThe aim of this study was to investigate the relationship between the eventual synthesis of PRL and PRLr isoforms with the inflammatory response in monocytes. We used THP-1 and monocytes isolated from healthy subjects stimulated with lipopolysaccharide (LPS). Western blot, real time PCR and immunocytochemistry were performed to identify both molecules. The bioactivity of the PRL was assessed using a bioassay and ELISA to detect pro inflammatory cytokines.

resultsPRLr mRNA and PRL mRNA were synthesized in THP-1 monocytes activated with LPS with peaks of 300-fold and 130-fold, respectively. The long (100 kDa) and the intermediate (50 kDa) isoforms of PRLr and big PRL (60 kDa) were time-dependent upregulated for monocytes stimulated with LPS. This expression was confirmed in monocytes from healthy subjects. The PRLr intermediate isoform and the big PRL were found soluble in the culture media and later in the nucleus in THP-1 monocytes stimulated with LPS. Big PRL released by monocytes showed bioactivity in Nb2 Cells, and both PRL and PRLr, synthesized by monocytes were related with levels of nitrites and proinflammatory citokines.

conclusionsOur results suggest the expression of a full-autocrine loop of PRL enhances the inflammatory response in activated monocytes. This response mediated by big PRL may contribute to the eradication of potential pathogens during innate immune response in monocytes but may also contribute to inflammatory disorders.

Identifiers

PMID23731754
PMCPMC3716533
OpenAlexW2131707604

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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.