Evidence map›Paper›PMID 20167656›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2010

Adenosine receptor A2A deficiency in leukocytes increases arterial neointima formation in apolipoprotein E-deficient mice.

Huan Wang, Weiyu Zhang, Rong Tang, Chuhong Zhu, Christoph Bucher, Bruce R Blazar, Jian-Guo Geng, Chunxiang Zhang, Joel Linden, Chaodong Wu and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.6field-weighted citation impact, top 12% 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

9 citing papers in PubMed, 20 citations in OpenAlex.

  1. APurinergic signalling · 2022
    Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. A2 adenosine receptors and vascular pathologies.Arteriosclerosis, thrombosis, and vascular biology · 2012
    Review
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

11 authors at 2 institutions in 1 country.

Huan WangDepartment of Medicine, University of Minnesota, Minneapolis, USA.
Weiyu Zhang
Rong Tang
Chuhong Zhu
Christoph Bucher
Bruce R Blazar
Jian-Guo Geng
Chunxiang Zhang
Joel Linden
Chaodong Wu
Yuqing Huo
University of Virginia Health System · USRutgers New Jersey Medical School

Funding

Role of miR-145 in Vascular Smooth Muscle Cell BiologyRole ofR01HL095707 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI ZHANG, CHUNXIANG · 2010 to 2013
$1.5M
MPO and NO signaling in neointima formationR01HL080133 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI ZHANG, CHUNXIANG · 2006 to 2010
$1.5M
Leukocyte C2GIcNAcT-I in atherosclerosisR01HL080569 · NHLBI · UNIVERSITY OF MINNESOTA · PI HUO, YUQING · 2006 to 2009
$1.4M
Inhibition of leukocyte C2GlcNAcT--l reduces thrombosisR01HL078679 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI HUO, YUQING · 2004 to 2007
$1.2M
NHLBI NIH HHS HL080569NHLBI NIH HHS HL78679NHLBI NIH HHS R01 HL078679NHLBI NIH HHS R01 HL080133NHLBI NIH HHS R01 HL080569NHLBI NIH HHS R01 HL095707
6 · The paper itself

Abstract

objectiveTo use the mice deficient in both adenosine receptor A(2A)(A(2A)R(-/-)) and apolipoprotein E (apoE(-/-)) to investigate the role of A(2A)R in mediating the interactions of leukocytes with injured arterial walls and the formation of arterial neointima induced by a guide wire. METHODS AND

resultsIn apoE(-/-) mice, A(2A)R deficiency increased the size of the arterial neointima in injured carotid arteries by 83%. Arterial neointima formation was also enhanced in chimeric mice that underwent bone marrow transplantation (these mice lacked A(2A)R in their bone marrow-derived cells). Epifluorescence intravital microscopy showed that neutrophil rolling and adherence to the injured arterial area were enhanced by 80% and 110% in A(2A)R(-/-)/apoE(-/-) mice, respectively. This phenomenon occurred even though the protein levels of homing molecules on A(2A)R-deficient neutrophils were unchanged from those of wild-type neutrophils. A(2A)R-deficient neutrophils exhibited an increase in the phosphorylation of p38 mitogen-activated protein kinase, P-selectin glycoprotein ligand-1 (PSGL-1) clustering, and the affinity of b(2) integrins. The inhibition of p38 phosphorylation abrogated the increased PSGL-1 clustering and beta(2) integrin affinity, thus reversing the increased homing ability of A(2A)R-deficient leukocytes.

conclusionA(2A)R plays a complex role in inflammation and tissue injury. The deficiency of A(2A)R enhances the homing ability of leukocytes and increases the formation of the arterial neointima after injury. A(2A)R antagonists are being tested for the treatment of neurodegenerative and other chronic diseases. An evaluation of the effect of A(2A)R antagonists on arterial restenosis after arterial angioplasty should be conducted.

Indexed as

Cell ProliferationNeutrophil InfiltrationAnimalsApolipoproteins EBone Marrow TransplantationCarotid ArteriesCarotid Artery InjuriesCD18 AntigensDisease Models, AnimalHyperplasiaLeukocyte RollingMaleMembrane GlycoproteinsMiceMice, Inbred C57BLMice, KnockoutApolipoproteins ECD18 AntigensMembrane Glycoproteinsp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsP-selectin ligand proteinReceptor, Adenosine A2A

Identifiers

PMID20167656
PMCPMC2860310
OpenAlexW2139777759

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.