Evidence map›Paper›PMID 23901069›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2013

Regulation of ecto-apyrase CD39 (ENTPD1) expression by phosphodiesterase III (PDE3).

Amy E Baek, Yogendra Kanthi, Nadia R Sutton, Hui Liao, David J Pinsky

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Ectonucleotidase Modulation of Lymphocyte Function in Gut and Liver.Frontiers in cell and developmental biology · 2020
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. CD39 improves survival in microbial sepsis by attenuating systemic inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
    Article
  13. Article
  14. Review
  15. 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

5 authors at 3 institutions in 1 country.

Amy E Baek17240 Medical Science Research Bldg. III, 1150 W. Medical Center Dr., Ann Arbor, MI 48109, USA. abaek@umich.edu.
Yogendra Kanthi
Nadia R Sutton
Hui Liao
David J Pinsky
Michigan Medicine · USAnn Arbor VA Medical Center · USUniversity of Michigan–Ann Arbor · US

Funding

TRAINING IN MOLECULAR AND CELLULAR CARDIOLOGYT32HL007853 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI David J. Pinsky · 1996 to 2026
$11.6M
SYTEMS AND INTEGRATIVE BIOLOGYT32GM008322 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LOW, MALCOLM JAMES · 1990 to 2020
$5.7M
NHLBI NIH HHS L30 HL115712NHLBI NIH HHS T32 HL007853NIGMS NIH HHS T32 GM008322
6 · The paper itself

Abstract

The ectoenzyme CD39 suppresses thrombosis and inflammation by suppressing ATP and ADP to AMP. However, mechanisms of CD39 transcriptional and post-translational regulation are not well known. Here we show that CD39 levels are modulated by inhibition of phosphodiesterase 3 (PDE3). RAW macrophages and human umbilical vein endothelial cells (HUVECs) were treated with the PDE3 inhibitors cilostazol and milrinone, then analyzed using qRT-PCR, immunoprecipitation/Western blot, immunofluorescent staining, radio-thin-layer chromatography, a malachite green assay, and ELISA. HUVECs expressed elevated CD39 protein (2-fold [P<0.05] for cilostazol and 2.5-fold [P<0.01] for milrinone), while macrophage CD39 mRNA and protein were both elevated after PDE3 inhibition. HUVEC ATPase activity increased by 25% with cilostazol and milrinone treatment (P<0.05 and P<0.01, respectively), as did ADPase activity (47% and 61%, P<0.001). There was also a dose-dependent elevation of soluble CD39 after treatment with 8-Br-cAMP, with maximal elevation of 60% more CD39 present compared to controls (1 mM, P<0.001). Protein harvested after 8-Br-cAMP treatment showed that ubiquitination of CD39 was decreased by 43% compared to controls. A DMSO or PBS vehicle control was included for each experiment based on solubility of cilostazol, milrinone, and 8-Br-cAMP. These results indicate that PDE3 inhibition regulates endothelial CD39 at a post-translational level.

Indexed as

Gene Expression Regulation, EnzymologicTranscription, Genetic8-Bromo Cyclic Adenosine MonophosphateAdenosine TriphosphatasesAntigens, CDApyraseCilostazolCyclic Nucleotide Phosphodiesterases, Type 3Enzyme InhibitorsHumansHuman Umbilical Vein Endothelial CellsMacrophagesMilrinoneTetrazolesUbiquitination8-Bromo Cyclic Adenosine MonophosphateAdenosine TriphosphatasesAntigens, CDApyraseCD39 antigenCilostazolCyclic Nucleotide Phosphodiesterases, Type 3Enzyme InhibitorsMilrinoneTetrazolescAMPendotheliumvascular homeostasis

Identifiers

PMID23901069
PMCPMC3804755
OpenAlexW2086357328

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.