Evidence map›Paper›PMID 21622827›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2011

2',3'-cAMP, 3'-AMP, and 2'-AMP inhibit human aortic and coronary vascular smooth muscle cell proliferation via A2B receptors.

Edwin K Jackson, Jin Ren, Delbert G Gillespie

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  5. 2',3'-cGMP exists in vivo and comprises a 2',3'-cGMP-guanosine pathway.American journal of physiology. Regulatory, integrative and comparative physiology · 2019
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  15. In vivo cardiovascular pharmacology of 2',3'-cAMP, 2'-AMP, and 3'-AMP in the rat.The Journal of pharmacology and experimental therapeutics · 2013
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. The 2',3'-cAMP-adenosine pathway.American journal of physiology. Renal physiology · 2011
    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

3 authors at 1 institution in 1 country.

Edwin K JacksonDept. of Pharmacology and Chemical Biology, Univ. of Pittsburgh School of Medicine, 100 Technology Drive, Rm. 514, Pittsburgh, PA 15219-3130, USA. edj@pitt.edu
Jin Ren
Delbert G Gillespie
University of Pittsburgh · US

Funding

Single Nephron and MetabolomicsP30DK079307 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KLEYMAN, THOMAS R · 2008 to 2022
$13.4M
Role of Renal Dipeptidyl Peptidase IVR01HL069846 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI JACKSON, EDWIN KERRY · 2003 to 2020
$6.6M
The Renal 2',3'-cAMP-Adenosine PathwayR01DK068575 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI JACKSON, EDWIN KERRY · 2005 to 2016
$4.0M
NHLBI NIH HHS HL-069846NIDDK NIH HHS DK-068575NIDDK NIH HHS DK-079307
6 · The paper itself

Abstract

Rat vascular smooth muscle cells (VSMCs) from renal microvessels metabolize 2',3'-cAMP to 2'-AMP and 3'-AMP, and these AMPs are converted to adenosine that inhibits microvascular VSMC proliferation via A(2B) receptors. The goal of this study was to test whether this mechanism also exists in VSMCs from conduit arteries and whether it is similarly expressed in human vs. rat VSMCs. Incubation of rat and human aortic VSMCs with 2',3'-cAMP concentration-dependently increased levels of 2'-AMP and 3'-AMP in the medium, with a similar absolute increase in 2'-AMP vs. 3'-AMP. In contrast, in human coronary VSMCs, 2',3'-cAMP increased 2'-AMP levels yet had little effect on 3'-AMP levels. In all cell types, 2',3'-cAMP increased levels of adenosine, but not 5'-AMP, and 2',3'-AMP inhibited cell proliferation. Antagonism of A(2B) receptors (MRS-1754), but not A(1) (1,3-dipropyl-8-cyclopentylxanthine), A(2A) (SCH-58261), or A(3) (VUF-5574) receptors, attenuated the antiproliferative effects of 2',3'-cAMP. In all cell types, 2'-AMP, 3'-AMP, and 5'-AMP increased adenosine levels, and inhibition of ecto-5'-nucleotidase blocked this effect of 5'-AMP but not that of 2'-AMP nor 3'-AMP. Also, 2'-AMP, 3'-AMP, and 5'-AMP, like 2',3'-cAMP, exerted antiproliferative effects that were abolished by antagonism of A(2B) receptors with MRS-1754. In conclusion, VSMCs from conduit arteries metabolize 2',3'-cAMP to AMPs, which are metabolized to adenosine. In rat and human aortic VSMCs, both 2'-AMP and 3'-AMP are involved in this process, whereas, in human coronary VSMCs, 2',3'-cAMP is mainly converted to 2'-AMP. Because adenosine inhibits VSMC proliferation via A(2B) receptors, local vascular production of 2',3'-cAMP may protect conduit arteries from atherosclerosis.

Indexed as

Cell ProliferationAdenine NucleotidesAdenosineAdenosine A2 Receptor AntagonistsAdenosine MonophosphateAnalysis of VarianceAnimalsAortaCells, CulturedCoronary VesselsDown-RegulationHumansMaleMuscle, Smooth, VascularMyocytes, Smooth MuscleRats2',3'-cyclic AMPAdenine NucleotidesAdenosineAdenosine A2 Receptor AntagonistsAdenosine MonophosphateReceptor, Adenosine A2B

Identifiers

PMID21622827
PMCPMC3154660
OpenAlexW2114642011

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.