Evidence map›Paper›PMID 7708708›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1995

Ca(2+)-inhibitable adenylyl cyclase modulates pulmonary artery endothelial cell cAMP content and barrier function.

T Stevens, Y Nakahashi, D N Cornfield, I F McMurtry, D M Cooper, D M Rodman

Open access · greenAbstract readComparative Study
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 80 citations in OpenAlex.

  1. Infection promotes Ser-214 phosphorylation important for generation of cytotoxic tau variants.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
  2. Review
  3. cAMP signaling primes lung endothelial cells to activate caspase-1 duringAmerican journal of physiology. Lung cellular and molecular physiology · 2020
    Article
  4. PGEAmerican journal of physiology. Renal physiology · 2017
    Article
  5. Article
  6. Review
  7. Article
  8. Adenylyl cyclase VI mediates vasopressin-stimulated ENaC activity.Journal of the American Society of Nephrology : JASN · 2013
    Article
  9. Article
  10. Article
  11. Article
  12. Filamin A is a phosphorylation target of membrane but not cytosolic adenylyl cyclase activity.American journal of physiology. Lung cellular and molecular physiology · 2011
    Article
  13. Emerging themes of cAMP regulation of the pulmonary endothelial barrier.American journal of physiology. Lung cellular and molecular physiology · 2011
    Review
  14. Article
  15. Article
  16. Article
  17. Soluble adenylyl cyclase-dependent microtubule disassembly reveals a novel mechanism of endothelial cell retraction.American journal of physiology. Lung cellular and molecular physiology · 2009
    Article
  18. Review
  19. Review
  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

6 authors at 1 institution in 1 country.

T StevensDepartment of Anesthesiology, University of Colorado Health Sciences Center, Denver 80262, USA.
Y Nakahashi
D N Cornfield
I F McMurtry
D M Cooper
D M Rodman
University of Colorado Health · US

Funding

Translational Pulmonary Vascular Biology ProgramT32HL007171 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI Sonia Castro Flores, Tim Lahm · 1985 to 2026
$9.4M
NHLBI NIH HHS HL-07171NHLBI NIH HHS HL-14985NHLBI NIH HHS HL-48036
6 · The paper itself

Abstract

Maintenance by the endothelium of a semi-permeable barrier is critically important in the exchange of oxygen and carbon dioxide in the lung. Intracellular free Ca2+ ([Ca2+]i) and cAMP are principal determinants of endothelial cell barrier function through their mutually opposing actions on endothelial retraction. However, details of the mechanisms of this antagonism are lacking. The recent discovery that certain adenylyl cyclases (EC 4.6.1.1) could be acutely inhibited by Ca2+ in the intracellular concentration range provided one possible mechanism whereby elevated [Ca2+]i could decrease cAMP content. This possibility was explored in pulmonary artery endothelial cells. The results indicate that a type VI Ca(2+)-inhibitable adenylyl cyclase exists in pulmonary artery endothelial cells and is modulated by physiological changes in [Ca2+]i. Furthermore, the results suggest the inverse relationship between [Ca2+]i and cAMP that is established by Ca(2+)-inhibitable adenylyl cyclase plays a critical role in modulating pulmonary artery endothelial cell permeability. These data provide evidence that susceptibility to inhibition of adenylyl cyclase by Ca2+ can be exploited in modulating a central physiological process.

Indexed as

Gene ExpressionAdenylyl CyclasesAmino Acid SequenceAnimalsBradykininCalciumCattleCell MembraneCells, CulturedCyclic AMPDNA, ComplementaryDogsEndothelium, VascularFura-2HumansIonomycinAdenylyl CyclasesBradykininCalciumCyclic AMPDNA, ComplementaryFura-2IonomycinLanthanumManganeseRNA, Messenger

Identifiers

PMID7708708
PMCPMC42285
OpenAlexW2090092318

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.