Evidence map›Paper›PMID 25608528›Full record

ArticleCirculation research2015

Role of cAMP-phosphodiesterase 1C signaling in regulating growth factor receptor stability, vascular smooth muscle cell growth, migration, and neointimal hyperplasia.

Yujun Cai, David J Nagel, Qian Zhou, Katherine D Cygnar, Haiqing Zhao, Faqian Li, Xinchun Pi, Peter A Knight, Chen Yan

Abstract read
In one paragraph

Article in Circulation research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
8.3field-weighted citation impact, top 2% 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

61 citing papers in PubMed, 92 citations in OpenAlex.

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  16. Long Noncoding RNACirculation · 2021
    Article
  17. Review
  18. Article
  19. Article
  20. Cyclic nucleotide phosphodiesterase 1C contributes to abdominal aortic aneurysm.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article

1 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Yujun CaiFrom the Department of Medicine, Aab Cardiovascular Research Institute (Y.C., D.J.N., Q.Z., C.Y.), Department of Pathology and Laboratory Medicine (F.L.), and Department of Surgery (P.A.K.), School of Medicine and Dentistry, University of Rochester, NY; Department of Biology, Johns Hopkins University, Baltimore, MD (K.D.C., H.Z.); and Department of Medicine, Athero and Lipo Cardiovascular Research Institute, Baylor College of Medicine, Houston, TX (X.P.).
David J NagelFrom the Department of Medicine, Aab Cardiovascular Research Institute (Y.C., D.J.N., Q.Z., C.Y.), Department of Pathology and Laboratory Medicine (F.L.), and Department of Surgery (P.A.K.), School of Medicine and Dentistry, University of Rochester, NY; Department of Biology, Johns Hopkins University, Baltimore, MD (K.D.C., H.Z.); and Department of Medicine, Athero and Lipo Cardiovascular Research Institute, Baylor College of Medicine, Houston, TX (X.P.).
Qian ZhouFrom the Department of Medicine, Aab Cardiovascular Research Institute (Y.C., D.J.N., Q.Z., C.Y.), Department of Pathology and Laboratory Medicine (F.L.), and Department of Surgery (P.A.K.), School of Medicine and Dentistry, University of Rochester, NY; Department of Biology, Johns Hopkins University, Baltimore, MD (K.D.C., H.Z.); and Department of Medicine, Athero and Lipo Cardiovascular Research Institute, Baylor College of Medicine, Houston, TX (X.P.).
Katherine D CygnarFrom the Department of Medicine, Aab Cardiovascular Research Institute (Y.C., D.J.N., Q.Z., C.Y.), Department of Pathology and Laboratory Medicine (F.L.), and Department of Surgery (P.A.K.), School of Medicine and Dentistry, University of Rochester, NY; Department of Biology, Johns Hopkins University, Baltimore, MD (K.D.C., H.Z.); and Department of Medicine, Athero and Lipo Cardiovascular Research Institute, Baylor College of Medicine, Houston, TX (X.P.).
Haiqing ZhaoFrom the Department of Medicine, Aab Cardiovascular Research Institute (Y.C., D.J.N., Q.Z., C.Y.), Department of Pathology and Laboratory Medicine (F.L.), and Department of Surgery (P.A.K.), School of Medicine and Dentistry, University of Rochester, NY; Department of Biology, Johns Hopkins University, Baltimore, MD (K.D.C., H.Z.); and Department of Medicine, Athero and Lipo Cardiovascular Research Institute, Baylor College of Medicine, Houston, TX (X.P.).
Faqian LiFrom the Department of Medicine, Aab Cardiovascular Research Institute (Y.C., D.J.N., Q.Z., C.Y.), Department of Pathology and Laboratory Medicine (F.L.), and Department of Surgery (P.A.K.), School of Medicine and Dentistry, University of Rochester, NY; Department of Biology, Johns Hopkins University, Baltimore, MD (K.D.C., H.Z.); and Department of Medicine, Athero and Lipo Cardiovascular Research Institute, Baylor College of Medicine, Houston, TX (X.P.).
Xinchun PiFrom the Department of Medicine, Aab Cardiovascular Research Institute (Y.C., D.J.N., Q.Z., C.Y.), Department of Pathology and Laboratory Medicine (F.L.), and Department of Surgery (P.A.K.), School of Medicine and Dentistry, University of Rochester, NY; Department of Biology, Johns Hopkins University, Baltimore, MD (K.D.C., H.Z.); and Department of Medicine, Athero and Lipo Cardiovascular Research Institute, Baylor College of Medicine, Houston, TX (X.P.).
Peter A KnightFrom the Department of Medicine, Aab Cardiovascular Research Institute (Y.C., D.J.N., Q.Z., C.Y.), Department of Pathology and Laboratory Medicine (F.L.), and Department of Surgery (P.A.K.), School of Medicine and Dentistry, University of Rochester, NY; Department of Biology, Johns Hopkins University, Baltimore, MD (K.D.C., H.Z.); and Department of Medicine, Athero and Lipo Cardiovascular Research Institute, Baylor College of Medicine, Houston, TX (X.P.).
Chen YanFrom the Department of Medicine, Aab Cardiovascular Research Institute (Y.C., D.J.N., Q.Z., C.Y.), Department of Pathology and Laboratory Medicine (F.L.), and Department of Surgery (P.A.K.), School of Medicine and Dentistry, University of Rochester, NY; Department of Biology, Johns Hopkins University, Baltimore, MD (K.D.C., H.Z.); and Department of Medicine, Athero and Lipo Cardiovascular Research Institute, Baylor College of Medicine, Houston, TX (X.P.). chen_yan@urmc.rochester.edu.
Johns Hopkins University · US

Funding

Regulation of Olfactory Signal TransductionR01DC007395 · NIDCD · JOHNS HOPKINS UNIVERSITY · PI ZHAO, HAIQING · 2008 to 2016
$3.5M
Regulation and Function of Phosphodiesterase in the HeartR01HL088400 · NHLBI · UNIVERSITY OF ROCHESTER · PI YAN, CHEN · 2008 to 2018
$3.1M
Nuclear beta-catenin signaling in the heartR01HL111480 · NHLBI · UNIVERSITY OF ROCHESTER · PI LI, FAQIAN · 2012 to 2016
$1.9M
LRP1 and endothelial functionR01HL112890 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PI, XINCHUN · 2013 to 2017
$1.9M
Function and Regulation of Phosphodiesterase in AtherogenesisR01HL111291 · NHLBI · UNIVERSITY OF ROCHESTER · PI YAN, CHEN · 2013 to 2016
$1.5M
NHLBI NIH HHS HL088400NHLBI NIH HHS HL111291NHLBI NIH HHS R01 HL088400NHLBI NIH HHS R01 HL111291NHLBI NIH HHS R01 HL111480NHLBI NIH HHS R01 HL112890NIDCD NIH HHS R01 DC007395
6 · The paper itself

Abstract

rationaleNeointimal hyperplasia characterized by abnormal accumulation of vascular smooth muscle cells (SMCs) is a hallmark of occlusive disorders such as atherosclerosis, postangioplasty restenosis, vein graft stenosis, and allograft vasculopathy. Cyclic nucleotides are vital in SMC proliferation and migration, which are regulated by cyclic nucleotide phosphodiesterases (PDEs).

objectiveOur goal is to understand the regulation and function of PDEs in SMC pathogenesis of vascular diseases. METHODS AND

resultsWe performed screening for genes differentially expressed in normal contractile versus proliferating synthetic SMCs. We observed that PDE1C expression was low in contractile SMCs but drastically elevated in synthetic SMCs in vitro and in various mouse vascular injury models in vivo. In addition, PDE1C was highly induced in neointimal SMCs of human coronary arteries. More importantly, injury-induced neointimal formation was significantly attenuated by PDE1C deficiency or PDE1 inhibition in vivo. PDE1 inhibition suppressed vascular remodeling of human saphenous vein explants ex vivo. In cultured SMCs, PDE1C deficiency or PDE1 inhibition attenuated SMC proliferation and migration. Mechanistic studies revealed that PDE1C plays a critical role in regulating the stability of growth factor receptors, such as PDGF receptor β (PDGFRβ) known to be important in pathological vascular remodeling. PDE1C interacts with low-density lipoprotein receptor-related protein-1 and PDGFRβ, thus regulating PDGFRβ endocytosis and lysosome-dependent degradation in an low-density lipoprotein receptor-related protein-1-dependent manner. A transmembrane adenylyl cyclase cAMP-dependent protein kinase cascade modulated by PDE1C is critical in regulating PDGFRβ degradation.

conclusionsThese findings demonstrated that PDE1C is an important regulator of SMC proliferation, migration, and neointimal hyperplasia, in part through modulating endosome/lysosome-dependent PDGFRβ protein degradation via low-density lipoprotein receptor-related protein-1.

Indexed as

AnimalsCarotid Artery InjuriesCell DivisionCell MovementCells, CulturedCyclic AMPCyclic Nucleotide Phosphodiesterases, Type 1EndocytosisEnzyme InductionHumansLow Density Lipoprotein Receptor-Related Protein-1LysosomesMaleMiceMice, Inbred C57BLMice, KnockoutCyclic AMPCyclic Nucleotide Phosphodiesterases, Type 1Low Density Lipoprotein Receptor-Related Protein-1LRP1 protein, humanPDE1C protein, humanPde1C protein, mouseReceptor, Platelet-Derived Growth Factor betacyclic nucleotide phosphodiesterases, type 1Cneointima formationsmooth muscle cell

Identifiers

PMID25608528
PMCPMC4702253
OpenAlexW2163491292

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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.