Evidence map›Paper›PMID 33398666›Full record

ArticleMolecular and cellular biochemistry2021

Endocan, a novel inflammatory marker, is upregulated in human chondrocytes stimulated with IL-1 beta.

Michele Scuruchi, Angela D'Ascola, Angela Avenoso, Giuseppe Mandraffino, Salvatore Campo, Giuseppe M Campo

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2021. 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, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Extracellular Vesicles Derived fromInternational journal of molecular sciences · 2024
    Article
  9. Review
  10. Observational
  11. Article
  12. Article
  13. Article
  14. P2YCancers · 2022
    Article
  15. Article
  16. Article
  17. Endocan: A Key Player of Cardiovascular Disease.Frontiers in cardiovascular medicine · 2021
    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

6 authors at 1 institution in 1 country.

Michele Scuruchi *Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy. mscuruchi@unime.it.ORCID http://orcid.org/0000-0002-5282-1690
Angela D'Ascola *Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy.
Angela AvenosoDepartment of Biomedical and Dental Sciences and Morphofunctional Images, University of Messina, Messina, Italy.
Giuseppe MandraffinoDepartment of Clinical and Experimental Medicine, University of Messina, Messina, Italy.
Salvatore CampoDepartment of Biomedical and Dental Sciences and Morphofunctional Images, University of Messina, Messina, Italy.
Giuseppe M CampoDepartment of Clinical and Experimental Medicine, University of Messina, Messina, Italy.
University of Messina · IT

Funding

Università degli Studi di Messina FFABR_2019
6 · The paper itself

Abstract

Endocan is a circulating proteoglycan, involved in immunity, inflammation, and endothelial function. It has been recently suggested as a biomarker of inflammation, increased angiogenesis, and cancer. In vitro studies have shown that endocan expression could be upregulated by inflammatory cytokines and proangiogenic molecules. High endocan levels were also shown in arthritic joint tissues and particularly in sites characterized by severe inflammation. This study was performed to evaluate endocan expression in chondrocytes stimulated with IL-ß. mRNA and related protein production were measured for endocan, TNF-α, and IL-6. NF-kB activity was also evaluated. IL-1ß treatment induced a significant upregulation of both endocan and the inflammatory parameters as well as NF-kB activity. The treatment of chondrocytes with the specific NF-kB inhibitor before IL-1ß stimulation was able to reduce endocan and the inflammatory markers over-expression. The results of our study indicated that endocan is also expressed in human chondrocytes; furthermore, consistent with previous results in other cell types and tissues, IL-1ß-induced inflammatory response involves the expression of endocan through NF-kB activation. In this context, endocan seems to be an important inflammatory marker associated with the activation of NF-kB pathway.

Indexed as

CartilageCell MovementChondrocytesHumansInflammationInterleukin-1betaInterleukin-6Neoplasm ProteinsNeovascularization, PathologicNF-kappa B p50 SubunitProteoglycansRecombinant ProteinsTranscription Factor RelATumor Necrosis Factor-alphaUp-RegulationESM1 protein, humanIL1B protein, humanIL6 protein, humanInterleukin-1betaInterleukin-6Neoplasm ProteinsNF-kappa B p50 SubunitNFKB1 protein, humanProteoglycansRecombinant ProteinsRELA protein, humanTranscription Factor RelATumor Necrosis Factor-alphaEndocanHuman chondrocytesInflammationNF-kBProteoglycans

Identifiers

PMID33398666
OpenAlexW3120316664

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.