Evidence map›Paper›PMID 27403036›Full record

ArticleMediators of inflammation2016

Regulator of Calcineurin 1 in Periodontal Disease.

Ulrike Peters, Eleni Solominidou, Yüksel Korkmaz, Stefan Rüttermann, Astrid Klocke, Thomas Frank Flemmig, Thomas Beikler

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Mediators of inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 36% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Downregulation of oxytocin-related genes in periodontitis.Frontiers in molecular neuroscience · 2022
    Article
  2. 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

7 authors at 4 institutions in 2 countries.

Ulrike PetersSection of Periodontics, Heinrich-Heine University, 40225 Düsseldorf, Germany.
Eleni SolominidouSection of Periodontics, Heinrich-Heine University, 40225 Düsseldorf, Germany.
Yüksel KorkmazInstitute for Experimental Dental Research and Oral Musculoskeletal Biology, Center for Biochemistry, University of Cologne, 50931 Cologne, Germany.
Stefan RüttermannDepartment of Operative Dentistry, Center for Dentistry and Oral Medicine (Carolinum), Goethe-University Frankfurt, 60596 Frankfurt, Germany.
Astrid KlockeSection of Periodontics, Heinrich-Heine University, 40225 Düsseldorf, Germany.
Thomas Frank FlemmigFaculty of Dentistry, The University of Hong Kong, Sai Ying Pun, Hong Kong.
Thomas BeiklerSection of Periodontics, Heinrich-Heine University, 40225 Düsseldorf, Germany.
Heinrich Heine University Düsseldorf · DEGoethe University Frankfurt · DEUniversity of Cologne · DEUniversity of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nuclear factor of activated T-cells (NFAT) and NF-kB pathway associated processes are involved in the pathogenesis of various inflammatory disorders, for example, periodontal disease. The activation of these pathways is controlled by the regulator of calcineurin 1 (RCAN1). The aim of this study was to elucidate the role of RCAN1 in periodontal disease. Healthy and inflamed periodontal tissues were analyzed by immunohistochemistry and immunofluorescence using specific rabbit polyclonal anti-RCAN1 antibodies. For expression analysis human umbilical vein endothelial cells (HUVEC) were used. HUVEC were incubated for 2 h with Vascular Endothelial Growth Factor (VEGF) or with wild type and laboratory strains of Porphyromonas gingivalis (P. gingivalis). Expression analysis of rcan1 and cox2 was done by real time PCR using specific primers for rcan1.4 and cox2. The expression of rcan1 was found to be significantly suppressed in endothelial cells of chronically inflamed periodontal tissues compared to healthy controls. Rcan1 and cox2 were significantly induced by VEGF and wild type and laboratory P. gingivalis strains. Interestingly, the magnitude of the rcan1 and cox2 induction was strain dependent. The results of this study indicate that RCAN1 is suppressed in endothelial cells of chronically inflamed periodontal tissues. During an acute infection, however, rcan1 seems to be upregulated in endothelial cells, indicating a modulating role in immune homeostasis of periodontal tissues.

Indexed as

Cyclooxygenase 2DNA-Binding ProteinsHumansHuman Umbilical Vein Endothelial CellsImmunohistochemistryIntracellular Signaling Peptides and ProteinsIn Vitro TechniquesMicroscopy, ConfocalMuscle ProteinsPeriodontal DiseasesPeriodontiumPorphyromonas gingivalisVascular Endothelial Growth Factor ACyclooxygenase 2DNA-Binding ProteinsIntracellular Signaling Peptides and ProteinsMuscle ProteinsPTGS2 protein, humanRCAN1 protein, humanVascular Endothelial Growth Factor A

Identifiers

PMID27403036
PMCPMC4925939
OpenAlexW2438028967

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.