Evidence map›Paper›PMID 19395666›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009

Soluble adenylyl cyclase-dependent microtubule disassembly reveals a novel mechanism of endothelial cell retraction.

Nutan Prasain, Mikhail Alexeyev, Ron Balczon, Troy Stevens

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

28 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. cUMP elicits interendothelial gap formation duringAmerican journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  3. Review
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  7. Article
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  9. Review
  10. Pseudomonas aeruginosa exoenzymes U and Y induce a transmissible endothelial proteinopathy.American journal of physiology. Lung cellular and molecular physiology · 2016
    Article
  11. Article
  12. Heterogeneity of pulmonary endothelial cyclic nucleotide response to Pseudomonas aeruginosa ExoY infection.American journal of physiology. Lung cellular and molecular physiology · 2015
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Studies on the cell biology of interendothelial cell gaps.American journal of physiology. Lung cellular and molecular physiology · 2012
    Review
  20. 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

4 authors at 1 institution in 1 country.

Nutan PrasainDepartments of Pharmacology, Center for Lung Biology, University of South Alabama, Mobile, Alabama 36688, USA.
Mikhail Alexeyev
Ron Balczon
Troy Stevens
University 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
Store-operated calcium entry: lung endothelial permeabilityR37HL060024 · NHLBI · UNIVERSITY OF SOUTH ALABAMA · PI STEVENS, TROY · 2010 to 2019
$3.9M
Store Operated Calcium Entry: Lung Endothelial PermeabilityR01HL060024 · NHLBI · UNIVERSITY OF SOUTH ALABAMA · PI STEVENS, TROY · 1998 to 2009
$3.0M
NHLBI NIH HHS HL-60024NHLBI NIH HHS HL-66299
6 · The paper itself

Abstract

Soluble adenylyl cyclase toxins, such as Pseudomonas aeruginosa exoY, generate a cAMP pool that retracts cell borders. However, the cytoskeletal basis by which this cAMP signal retracts cell borders is not known. We sought to determine whether activation of chimeric, soluble adenylyl cyclase I/II (sACI/II) reorganizes either microtubules or peripheral actin. Endothelial cells were stably transfected with either green fluorescent protein-labeled alpha-tubulin or beta-actin, and then infected with adenovirus to express sACI/II. Forskolin, which stimulates both the endogenously expressed transmembrane adenylyl cyclases and sACI/II, induced cell retraction accompanied by the reorganization of peripheral microtubules. However, cortical filamentous-actin (f-actin) did not reorganize into stress fibers, and myosin light-chain-20 phosphorylation was decreased. Isoproterenol, which activates endogenous adenylyl cyclases but does not activate sACI/II, did not induce endothelial cell gaps and did not influence microtubule or f-actin architecture. Thus, sACI/II generates a cAMP signal that reorganizes microtubules and induces cell retraction, without inducing f-actin stress fibers. These findings illustrate that endothelial cell gap formation can proceed without f-actin stress fiber formation, and provide mechanistic insight how bacterial adenylyl cyclase toxins reorganize the cytoskeleton to induce cell rounding.

Indexed as

Adenylyl CyclasesCell MembraneCell Membrane PermeabilityColforsinCyclic AMPCytosolEndothelial CellsEnzyme ActivationMicrotubulesSolubilityStress FibersAdenylyl CyclasesColforsinCyclic AMP

Identifiers

PMID19395666
PMCPMC2711814
OpenAlexW2035399266

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.