Evidence map›Paper›PMID 19389706›Full record

ArticleThe Journal of biological chemistry2009

Protein kinase A-regulated assembly of a MEF2{middle dot}HDAC4 repressor complex controls c-Jun expression in vascular smooth muscle cells.

Joseph W Gordon, Christina Pagiatakis, Jahan Salma, Min Du, John J Andreucci, Jianzhong Zhao, Guangpei Hou, Robert L Perry, Qinghong Dan, David Courtman and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
1.7field-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

41 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. FoxP1 Represses MEF2A in Striated Muscle.Molecular and cellular biology · 2024
    Article
  5. Article
  6. Article
  7. Knockdown of lncRNA H19 alleviates ox-LDL-induced HCAECs inflammation and injury by mediating miR-20a-5p/HDAC4 axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. The Therapeutic Strategy of HDAC6 Inhibitors in Lymphoproliferative Disease.International journal of molecular sciences · 2018
    Review
  16. Article
  17. Review
  18. Article
  19. TGF-βAmerican journal of physiology. Lung cellular and molecular physiology · 2017
    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

12 authors at 3 institutions in 1 country.

Joseph W GordonDepartment of Biology, York University, Toronto, Ontario M3J 1P3, Canada.
Christina Pagiatakis
Jahan Salma
Min Du
John J Andreucci
Jianzhong Zhao
Guangpei Hou
Robert L Perry
Qinghong Dan
David Courtman
Michelle P Bendeck
John C McDermott
York University · CASt. Michael's Hospital · CAUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular smooth muscle cells (VSMCs) maintain the ability to modulate their phenotype in response to changing environmental stimuli. This phenotype modulation plays a critical role in the development of most vascular disease states. In these studies, stimulation of cultured vascular smooth muscle cells with platelet-derived growth factor resulted in marked induction of c-jun expression, which was attenuated by protein kinase Cdelta and calcium/calmodulin-dependent protein kinase inhibition. Given that these signaling pathways have been shown to relieve the repressive effects of class II histone deacetylases (HDACs) on myocyte enhancer factor (MEF) 2 proteins, we ectopically expressed HDAC4 and observed repression of c-jun expression. Congruently, suppression of HDAC4 by RNA interference resulted in enhanced c-jun expression. Consistent with these findings, mutation of the MEF2 cis-element in the c-jun promoter resulted in promoter activation during quiescent conditions, suggesting that the MEF2 cis-element functions as a repressor in this context. Furthermore, we demonstrate that protein kinase A attenuates c-Jun expression by promoting the formation of a MEF2.HDAC4 repressor complex by inhibiting salt-inducible kinase 1. Finally, we document a physical interaction between c-Jun and myocardin, and we document that forced expression of c-Jun represses the ability of myocardin to activate smooth muscle gene expression. Thus, MEF2 and HDAC4 act to repress c-Jun expression in quiescent VSMCs, protein kinase A enhances this repression, and platelet-derived growth factor derepresses c-Jun expression through calcium/calmodulin-dependent protein kinases and novel protein kinase Cs. Regulation of this molecular "switch" on the c-jun promoter may thus prove critical for toggling between the activated and quiescent VSMC phenotypes.

Indexed as

Gene Expression RegulationAnimalsCell NucleusCyclic AMP-Dependent Protein KinasesHistone DeacetylasesMEF2 Transcription FactorsMiceModels, BiologicalMuscle, Smooth, VascularMyocardinMyogenic Regulatory FactorsNuclear ProteinsPromoter Regions, GeneticProto-Oncogene Proteins c-junRatsRNA InterferenceCyclic AMP-Dependent Protein KinasesHdac5 protein, mouseHistone DeacetylasesMef2a protein, mouseMEF2 Transcription FactorsMyocardinMyogenic Regulatory FactorsNuclear ProteinsProto-Oncogene Proteins c-junRNA, Small InterferingTrans-Activators

Identifiers

PMID19389706
PMCPMC2707197
OpenAlexW2042254753

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.