Evidence map›Paper›PMID 22116306›Full record

ArticleAmerican journal of physiology. Cell physiology2012

Assessment of cellular mechanisms contributing to cAMP compartmentalization in pulmonary microvascular endothelial cells.

Wei P Feinstein, Bing Zhu, Silas J Leavesley, Sarah L Sayner, Thomas C Rich

Abstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.3field-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

46 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Article
  3. GPCR signaling via cAMP nanodomains.The Biochemical journal · 2025
    Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. cAMP signaling: a remarkably regional affair.Trends in biochemical sciences · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. A multiscale model of the regulation of aquaporin 2 recycling.NPJ systems biology and applications · 2022
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Wei P FeinsteinCenter for Lung Biology, University of South Alabama, Mobile, Alabama 36688, USA.
Bing Zhu
Silas J Leavesley
Sarah L Sayner
Thomas C Rich
Molecular Research Institute · USUniversity of South Alabama · US

Funding

T-type Calcium Channels and von Willebrand Factor ReleaseP01HL066299 · NHLBI · UNIVERSITY OF SOUTH ALABAMA · PI ALVAREZ, DIEGO F. · 2001 to 2022
$34.6M
cAMP Phosphodiesterase and Lung Endothelial Cell PermeabilityR01HL094455 · NHLBI · UNIVERSITY OF SOUTH ALABAMA · PI RICH, THOMAS C · 2009 to 2010
$847k
Request for a Spectral Confocal MicroscopeS10RR027535 · NCRR · UNIVERSITY OF SOUTH ALABAMA · PI RICH, THOMAS C · 2010 to 2010
$397k
NCRR NIH HHS S10 RR027535NCRR NIH HHS S10RR027535NHLBI NIH HHS P01 HL066299NHLBI NIH HHS R01 HL094455NHLBI NIH HHS R01HL094455PHS HHS P01H066299
6 · The paper itself

Abstract

Cyclic AMP signals encode information required to differentially regulate a wide variety of cellular responses; yet it is not well understood how information is encrypted within these signals. An emerging concept is that compartmentalization underlies specificity within the cAMP signaling pathway. This concept is based on a series of observations indicating that cAMP levels are distinct in different regions of the cell. One such observation is that cAMP production at the plasma membrane increases pulmonary microvascular endothelial barrier integrity, whereas cAMP production in the cytosol disrupts barrier integrity. To better understand how cAMP signals might be compartmentalized, we have developed mathematical models in which cellular geometry as well as total adenylyl cyclase and phosphodiesterase activities were constrained to approximate values measured in pulmonary microvascular endothelial cells. These simulations suggest that the subcellular localizations of adenylyl cyclase and phosphodiesterase activities are by themselves insufficient to generate physiologically relevant cAMP gradients. Thus, the assembly of adenylyl cyclase, phosphodiesterase, and protein kinase A onto protein scaffolds is by itself unlikely to ensure signal specificity. Rather, our simulations suggest that reductions in the effective cAMP diffusion coefficient may facilitate the formation of substantial cAMP gradients. We conclude that reductions in the effective rate of cAMP diffusion due to buffers, structural impediments, and local changes in viscosity greatly facilitate the ability of signaling complexes to impart specificity within the cAMP signaling pathway.

Indexed as

Models, BiologicalAdenylyl CyclasesAnimalsCell CompartmentationCell Culture TechniquesCell MembraneComputer SimulationCyclic AMPCyclic AMP-Dependent Protein KinasesCytosolEndothelial CellsLungPhosphoric Diester HydrolasesRatsReceptors, G-Protein-CoupledSignal TransductionAdenylyl CyclasesCyclic AMPCyclic AMP-Dependent Protein KinasesPhosphoric Diester HydrolasesReceptors, G-Protein-Coupled

Identifiers

PMID22116306
PMCPMC3311237
OpenAlexW2097898429

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.