Evidence map›Paper›PMID 30440036›Full record

ArticlePloS one2018

Cytokine-induced cysteine- serine-rich nuclear protein-1 (CSRNP1) selectively contributes to MMP1 expression in human chondrocytes.

Christopher D Macdonald, Adrian M D Falconer, Chun Ming Chan, David J Wilkinson, Andrew Skelton, Louise Reynard, Gary J Litherland, G Nicholas Europe-Finner, Andrew D Rowan

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.3field-weighted citation impact, top 45% 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

7 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
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  5. Review
  6. Article
  7. TheFrontiers in oncology · 2021
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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 1 institution in 1 country.

Christopher D MacdonaldSkeletal Research Group, Institute of Genetic Medicine, Newcastle University, Newcastle-upon-Tyne, United Kingdom.
Adrian M D FalconerSkeletal Research Group, Institute of Genetic Medicine, Newcastle University, Newcastle-upon-Tyne, United Kingdom.
Chun Ming ChanSkeletal Research Group, Institute of Genetic Medicine, Newcastle University, Newcastle-upon-Tyne, United Kingdom.
David J WilkinsonSkeletal Research Group, Institute of Genetic Medicine, Newcastle University, Newcastle-upon-Tyne, United Kingdom.
Andrew SkeltonSkeletal Research Group, Institute of Genetic Medicine, Newcastle University, Newcastle-upon-Tyne, United Kingdom.
Louise ReynardSkeletal Research Group, Institute of Genetic Medicine, Newcastle University, Newcastle-upon-Tyne, United Kingdom.
Gary J LitherlandSkeletal Research Group, Institute of Genetic Medicine, Newcastle University, Newcastle-upon-Tyne, United Kingdom.
G Nicholas Europe-FinnerSkeletal Research Group, Institute of Genetic Medicine, Newcastle University, Newcastle-upon-Tyne, United Kingdom.
Andrew D RowanSkeletal Research Group, Institute of Genetic Medicine, Newcastle University, Newcastle-upon-Tyne, United Kingdom.ORCID 0000-0002-5338-1295
Newcastle University · GB

Funding

Arthritis Research UK 20199Medical Research Council MR/P020941/1
6 · The paper itself

Abstract

Irreversible cartilage collagen breakdown by the collagenolytic matrix metalloproteinases (MMPs)-1 and MMP-13 represents a key event in pathologies associated with tissue destruction such as arthritis. Inflammation is closely associated with such pathology and occurs in both rheumatoid and osteoarthritis making it highly relevant to the prevailing tissue damage that characterises these diseases. The inflammation-induced activating protein-1 (AP-1) transcription factor is an important regulator of both MMP1 and MMP13 genes with interplay between signalling pathways contributing to their expression. Here, we have examined the regulation of MMP1 expression, and using in vivo chromatin immunoprecipitation analyses we have demonstrated that cFos bound to the AP-1 cis element within the proximal MMP1 promoter only when the gene was transcriptionally silent as previously observed for MMP13. Subsequent small interfering RNA-mediated silencing confirmed however, that cFos significantly contributes to MMP1 expression. In contrast, silencing of ATF3 (a prime MMP13 modulator) did not affect MMP1 expression whilst silencing of the Wnt-associated regulator cysteine- serine-rich nuclear protein-1 (CSRNP1) resulted in substantial repression of MMP1 but not MMP13. Furthermore, following an early transient peak in expression of CSRNP1 at the mRNA and protein levels similar to that seen for cFOS, CSRNP1 expression subsequently persisted unlike cFOS. Finally, DNA binding assays indicated that the binding of CSRNP1 to the AP-1 consensus-like sequences within the proximal promoter regions of MMP1 and MMP13 was preferentially selective for MMP1 whilst activating transcription factor 3 (ATF3) binding was exclusive to MMP13. These data further extend our understanding of the previously reported differential regulation of these MMP genes, and strongly indicate that although cFos modulates the expression of MMP1/13, downstream factors such as CSRNP1 and ATF3 ultimately serve as transcriptional regulators in the context of an inflammatory stimulus for these potent collagenolytic MMPs.

Indexed as

Activating Transcription Factor 3Apoptosis Regulatory ProteinsCell NucleusCells, CulturedChondrocytesComputer SimulationGene Expression Regulation, EnzymologicHumansInterleukin-1Matrix Metalloproteinase 1Matrix Metalloproteinase 13Promoter Regions, GeneticProto-Oncogene Proteins c-fosTime FactorsTranscription, GeneticActivating Transcription Factor 3Apoptosis Regulatory ProteinsATF3 protein, humanCSRNP1 protein, humanInterleukin-1Matrix Metalloproteinase 1Matrix Metalloproteinase 13MMP13 protein, humanMMP1 protein, humanProto-Oncogene Proteins c-fos

Identifiers

PMID30440036
PMCPMC6237337
OpenAlexW2901845544

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.