Evidence map›Paper›PMID 21148428›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2011

Cyclic nucleotide phosphodiesterase 1 regulates lysosome-dependent type I collagen protein degradation in vascular smooth muscle cells.

Yujun Cai, Clint L Miller, David J Nagel, Kye-Im Jeon, Soyeon Lim, Pingjin Gao, Peter A Knight, Chen Yan

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Cyclic nucleotide phosphodiesterase 1C contributes to abdominal aortic aneurysm.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  6. Article
  7. Pharmacological modulation of the COPharmacology & therapeutics · 2018
    Review
  8. Article
  9. Review
  10. PDE1C deficiency antagonizes pathological cardiac remodeling and dysfunction.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  11. Cyclic nucleotide phosphodiesterase 1 and vascular aging.Clinical science (London, England : 1979) · 2015
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. 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

8 authors at 1 institution in 1 country.

Yujun CaiAab Cardiovascular Research Institute, University of Rochester, Rochester, NY 14642, USA.
Clint L Miller
David J Nagel
Kye-Im Jeon
Soyeon Lim
Pingjin Gao
Peter A Knight
Chen Yan
Shanghai Institute of Hypertension · CN

Funding

Vascular Inflammation and AtherosclerosisP01HL077789 · NHLBI · UNIVERSITY OF ROCHESTER · PI BERK, BRADFORD C · 2005 to 2009
$10.1M
Regulation and Function of Phosphodiesterase in the HeartR01HL088400 · NHLBI · UNIVERSITY OF ROCHESTER · PI YAN, CHEN · 2008 to 2018
$3.1M
NHLBI NIH HHS HL077789NHLBI NIH HHS HL088400NHLBI NIH HHS P01 HL077789NHLBI NIH HHS R01 HL088400
6 · The paper itself

Abstract

objectiveThe phenotypic modulation of vascular smooth muscle cells (VSMCs) to a synthetic phenotype is vital during pathological vascular remodeling and the development of various vascular diseases. An increase in type I collagen (collagen I) has been implicated in synthetic VSMCs, and cyclic nucleotide signaling is critical in collagen I regulation. Herein, we investigate the role and underlying mechanism of cyclic nucleotide phosphodiesterase 1 (PDE1) in regulating collagen I in synthetic VSMCs. METHODS AND

resultsThe PDE1 inhibitor IC86340 significantly reduced collagen I in human saphenous vein explants undergoing spontaneous remodeling via ex vivo culture. In synthetic VSMCs, high basal levels of intracellular and extracellular collagen I protein were markedly decreased by IC86340. This attenuation was due to diminished protein but not mRNA. Inhibition of lysosome function abolished the effect of IC86340 on collagen I protein expression. PDE1C but not PDE1A is the major isoform responsible for mediating the effects of IC86340. Bicarbonate-sensitive soluble adenylyl cyclase/cAMP signaling was modulated by PDE1C, which is critical in collagen I degradation in VSMCs.

conclusionsThese data demonstrate that PDE1C regulates soluble adenylyl cyclase/cAMP signaling and lysosome-mediated collagen I protein degradation, and they suggest that PDE1C plays a critical role in regulating collagen homeostasis during pathological vascular remodeling.

Indexed as

Adenylyl CyclasesAnimalsBicarbonatesCells, CulturedCollagen Type ICyclic AMPCyclic AMP-Dependent Protein KinasesCyclic GMP-Dependent Protein KinasesCyclic Nucleotide-Gated Cation ChannelsCyclic Nucleotide Phosphodiesterases, Type 1Guanine Nucleotide Exchange FactorsHumansLysosomesMuscle, Smooth, VascularMyocytes, Smooth MusclePhenotypeAdenylyl CyclasesBicarbonatesCollagen Type ICyclic AMPCyclic AMP-Dependent Protein KinasesCyclic GMP-Dependent Protein KinasesCyclic Nucleotide-Gated Cation ChannelsCyclic Nucleotide Phosphodiesterases, Type 1Guanine Nucleotide Exchange FactorsPde1a protein, ratPde1C protein, ratPhosphodiesterase Inhibitors

Identifiers

PMID21148428
PMCPMC4114343
OpenAlexW2150195517

What OpenQuestion holds

Textmetadata
LicenceTDM
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.