Evidence map›Paper›PMID 22619251›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2012

Adenylyl cyclase 2 selectively couples to E prostanoid type 2 receptors, whereas adenylyl cyclase 3 is not receptor-regulated in airway smooth muscle.

Amy S Bogard, Piyatilake Adris, Rennolds S Ostrom

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2012. 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
1.4field-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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Prostacyclin enlists AC6 to stop the clot.Journal of thrombosis and haemostasis : JTH · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Cross-Talk Between the Adenylyl Cyclase/cAMP Pathway and CaReviews of physiology, biochemistry and pharmacology · 2021
    Review
  10. Agonist-specific desensitization of PGENaunyn-Schmiedeberg's archives of pharmacology · 2020
    Article
  11. Article
  12. Effect of Adenylyl Cyclase Type 6 on Localized Production of cAMP byThe Journal of pharmacology and experimental therapeutics · 2019
    Article
  13. Cooperativity of E-prostanoid receptor subtypes in regulating signaling and growth inhibition in human airway smooth muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  14. PDE8 Is Expressed in Human Airway Smooth Muscle and Selectively Regulates cAMP Signaling by βAmerican journal of respiratory cell and molecular biology · 2018
    Article
  15. Review
  16. Compartmentalized cAMP responses to prostaglandin EPBritish journal of pharmacology · 2017
    Article
  17. Review
  18. Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Amy S BogardDepartment of Pharmacology, University of Tennessee Health Science Center, 874 Union Ave., Crowe 115, Memphis, TN 38163, USA.
Piyatilake Adris
Rennolds S Ostrom
University of Tennessee Health Science Center · US

Funding

Adenylyl cyclases in airway and GI smooth muscleR01HL079166 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI OSTROM, RENNOLDS S · 2006 to 2010
$1.7M
NHLBI NIH HHS HL079166NHLBI NIH HHS R01 HL079166
6 · The paper itself

Abstract

Adenylyl cyclases (ACs) are important regulators of airway smooth muscle function, because β-adrenergic receptor (βAR) agonists stimulate AC activity and cAMP production. We have previously shown in a number of cell types that AC6 selectively couples to βAR and these proteins are coexpressed in lipid rafts. We overexpressed AC2, AC3, and AC6 in mouse bronchial smooth muscle cells (mBSMCs) and human embryonic kidney (HEK)-293 cells by using recombinant adenoviruses and assessed their localization and regulation by various G protein-coupled receptors (GPCRs). AC3 and AC6 were expressed primarily in caveolin-rich fractions, whereas AC2 expression was excluded from these domains. AC6 expression enhanced cAMP production in response to isoproterenol but did not increase responses to butaprost, reflecting the colocalization of AC6 with β(2)AR but not E prostanoid type 2 receptor (EP(2)R) in lipid raft fractions. AC2 expression enhanced butaprost-stimulated cAMP production but had no effect on the β(2)AR-mediated response. AC3 did not couple to any GPCR tested. Forskolin-induced arborization of mBSMCs was assessed as a functional readout of cAMP signaling. Arborization was enhanced by overexpression of AC6 and AC3, but AC2 had no effect. GPCR-stimulated arborization mirrored the selective coupling observed for cAMP production. With the addition of the phosphodiesterase 4 (PDE4) inhibitor rolipram AC2 accelerated forskolin-stimulated arborization. Thus, AC2 selectively couples to EP(2)R, but signals from this complex are limited by PDE4 activity. AC3 does not seem to couple to GPCR in either mBSMCs or HEK-293 cells, so it probably exists in a distinct signaling domain in these cells.

Indexed as

Adenylyl CyclasesAlprostadilAnimalsBronchiCaveolinsCell Line, TransformedColforsinCyclic AMPCyclic Nucleotide Phosphodiesterases, Type 4HEK293 CellsHumansIsoproterenolMaleMiceMuscle, SmoothMyocytes, Smooth Muscleadenylate cyclase 3adenylyl cyclase 2Adenylyl CyclasesAlprostadilbutaprostCaveolinsColforsinCyclic AMPCyclic Nucleotide Phosphodiesterases, Type 4IsoproterenolReceptors, Adrenergic, beta-2Receptors, G-Protein-CoupledReceptors, Prostaglandin E, EP2 Subtype

Identifiers

PMID22619251
PMCPMC3400804
OpenAlexW2144391865

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.