Evidence map›Paper›PMID 24023832›Full record

ArticlePloS one2013

C-Fos regulation by the MAPK and PKC pathways in intervertebral disc cells.

Katsuya Yokoyama, Akihiko Hiyama, Fumiyuki Arai, Tadashi Nukaga, Daisuke Sakai, Joji Mochida

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

32 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Pharmaceuticals (Basel, Switzerland) · 2023
    Article
  8. Cytokine Imbalance as a Biomarker of Intervertebral Disk Degeneration.International journal of molecular sciences · 2023
    Review
  9. Article
  10. Review
  11. Single-cell RNA-sequencing atlas of bovine caudal intervertebral discs: Discovery of heterogeneous cell populations with distinct roles in homeostasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Journal of diabetes and metabolic disorders · 2020
    Article
  17. Article
  18. Review
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

Katsuya YokoyamaDepartment of Orthopaedic Surgery, Surgical Science, Tokai University School of Medicine, Kanagawa, Japan ; Research Center for Regenerative Medicine, Tokai University School of Medicine, Kanagawa, Japan.
Akihiko Hiyama
Fumiyuki Arai
Tadashi Nukaga
Daisuke Sakai
Joji Mochida
Tokai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe gene encoding c-fos is an important factor in the pathogenesis of joint disease in patients with osteoarthritis. However, it is unknown whether the signal mechanism of c-fos acts in intervertebral disc (IVD) cells. We investigated whether c-fos is activated in relation to mitogen-activated protein kinases (MAPKs) and the protein kinase C (PKC) pathway in nucleus pulposus (NP) cells. METHODOLOGY/

resultsReverse transcription-polymerase chain reaction and western blotting analyses were used to measure the expression of c-fos in rat IVD cells. Transfections were performed to determine the effects of c-fos on target gene activity. The effect of c-fos protein expression was examined in transfection experiments and in a 3- (4,5-dimethylthiazol-2-yl) -2,5-diphenyltetrazolium bromide cell viability assay. Phorbol 12-myristate 13-acetate (PMA), the most commonly used phorbol ester, binds to and activates protein kinase C (PKC), causing a wide range of effects in cells and tissues. PMA induced the expression of c-fos gene transcription and protein expression, and led to activation of the MAPK pathways in NP cells. The c-fos promoter was suppressed completely in the presence of the MAPK inhibitor PD98059, an inhibitor of the MEK/ERK kinase cascade, but not in the presence of SKF86002, SB202190, or SP600125. The effects of the PKC pathway on the transcriptional activity of the c-fos were evaluated. PKCγ and PKCδ suppressed the promoter activity of c-fos. Treatment with c-fos inhibited aggrecan and Col2 promoter activities and the expression of these genes in NP cells.

conclusionsThis study demonstrated, for the first time, that the MAPK and PKC pathways had opposing effects on the regulation of c-fos in NP cells. Thus, the expression of c-fos can be suppressed in the extracellular matrix of NP cells.

Indexed as

MAP Kinase Signaling SystemAnimalsCell ProliferationExtracellular MatrixFemaleIntervertebral DiscIntervertebral Disc DegenerationMitogen-Activated Protein KinasesProtein Kinase CProtein Kinase C-deltaProto-Oncogene Proteins c-fosRatsRats, Sprague-DawleyTetradecanoylphorbol AcetateTranscription Factor AP-1Transcription, GeneticMitogen-Activated Protein KinasesProtein Kinase CProtein Kinase C-deltaProto-Oncogene Proteins c-fosTetradecanoylphorbol AcetateTranscription Factor AP-1

Identifiers

PMID24023832
PMCPMC3759433
OpenAlexW2003053940

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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.