Evidence map›Paper›PMID 29911275›Full record

ArticleInflammation2018

Inflammation-Induced Epithelial-to-Mesenchymal Transition and GM-CSF Treatment Stimulate Mesenteric Mesothelial Cells to Transdifferentiate into Macrophages.

Sándor Katz, Viktória Zsiros, Nikolett Dóczi, Anna L Kiss

Abstract read
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In one paragraph

Article in Inflammation, 2018. 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
1.3field-weighted citation impact, top 22% 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, 25 citations in OpenAlex.

  1. Article
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  11. Article
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  13. Inflammation in Focus: The Beginning and the End.Pathology oncology research : POR · 2021
    Review
  14. Review
  15. Cellular and molecular events of inflammation induced transdifferentiation (EMT) and regeneration (MET) in mesenteric mesothelial cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
    Review
  16. Under inflammatory stimuli mesenteric mesothelial cells transdifferentiate into macrophages and produce pro-inflammatory cytokine IL-6.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Article
  17. 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

4 authors at 1 institution in 1 country.

Sándor KatzDepartment of Anatomy, Histology and Embryology, Semmelweis University, Tűzoltó u. 58, Budapest, 1094, Hungary.
Viktória ZsirosDepartment of Anatomy, Histology and Embryology, Semmelweis University, Tűzoltó u. 58, Budapest, 1094, Hungary.
Nikolett DócziDepartment of Anatomy, Histology and Embryology, Semmelweis University, Tűzoltó u. 58, Budapest, 1094, Hungary.
Anna L KissDepartment of Anatomy, Histology and Embryology, Semmelweis University, Tűzoltó u. 58, Budapest, 1094, Hungary. kiss.anna@med.semmelweis-univ.hu.
Semmelweis University · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In our previous work, we showed that during inflammation-induced epithelial-to-mesenchymal transition (EMT), mesenteric mesothelial cells express ED1 (pan-macrophage marker), indicating that they are transformed into macrophage-like cells. In this paper, we provide additional evidences about this transition by following the phagocytic activity and the TNFα production of mesenteric mesothelial cells during inflammation. Upon injection of India ink particles or fluorescent-labeled bioparticles (pHrodo) into the peritoneal cavity of rats pretreated with Freund's adjuvant, we found that mesothelial cells efficiently engulfed these particles. A similar increase of internalization could be observed by mesothelial cells in GM-CSF pretreated primary mesenteric culture. Since macrophages are the major producers of tumor necrosis factor, TNFα, we investigated expression level of TNFα during inflammation-induced EMT and found that TNFα was indeed expressed in these cells, reaching the highest level at the 5th day of inflammation. Since TNFα is one of the target genes of early growth response (EGR1) transcription factor, playing important role in monocyte-macrophage differentiation, expression of EGR1 in mesothelial cells was also investigated by Western blot and immunocytochemistry. While mesothelial cells did not express EGR1, a marked increase was observed in mesothelial cells by the time of inflammation. Parallel to this, nuclear translocation of EGR1 was shown by immunocytochemistry at the day 5 of inflammation. Caveolin-1 level was high and ERK1/2 became phosphorylated as the inflammation proceeded showing a slight decrease when the regeneration started. Our present data support the idea that under special stimuli, mesenteric mesothelial cells are able to transdifferentiate into macrophages, and this transition is regulated by the caveolin-1/ERK1/2/EGR1 signaling pathway.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsCaveolin 1Cell TransdifferentiationEarly Growth Response Protein 1Epithelial CellsGranulocyte-Macrophage Colony-Stimulating FactorInflammationMacrophagesMAP Kinase Signaling SystemMesenteryRatsSignal TransductionTumor Necrosis Factor-alphaCaveolin 1Early Growth Response Protein 1Granulocyte-Macrophage Colony-Stimulating FactorTumor Necrosis Factor-alphacaveolaeepithelial-to-mesenchymal cell transition (EMT)inflammationmesothelial cell-to-macrophage transition (MMT)phagocytosis

Identifiers

PMID29911275
OpenAlexW2808970206

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.