Evidence map›Paper›PMID 27422996›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016

Endothelial hyperpermeability in severe pulmonary arterial hypertension: role of store-operated calcium entry.

Chun Zhou, Mary I Townsley, Mikhail Alexeyev, Norbert F Voelkel, Troy Stevens

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Mechanisms of pulmonary vascular dysfunction in pulmonary hypertension and implications for novel therapies.American journal of physiology. Heart and circulatory physiology · 2022
    Review
  9. Review
  10. Role of store-operated Ca2+ entry in cardiovascular disease.Cell communication and signaling : CCS · 2022
    Review
  11. Review
  12. Article
  13. Inflammation in Pulmonary Arterial Hypertension.Advances in experimental medicine and biology · 2021
    Review
  14. Multiplexed, high-throughput measurements of cell contraction and endothelial barrier function.Laboratory investigation; a journal of technical methods and pathology · 2019
    Article
  15. Spontaneous pulmonary hypertension in genetic mouse models of natural killer cell deficiency.American journal of physiology. Lung cellular and molecular physiology · 2018
    Article
  16. Hemolysis-induced Lung Vascular Leakage Contributes to the Development of Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2018
    Article
  17. Article
  18. Mitochondrial dysfunction and pulmonary hypertension: cause, effect, or both.American journal of physiology. Lung cellular and molecular physiology · 2018
    Review
  19. Article
  20. When higher cholesterol is better: membrane cholesterol loss and endothelial CaAmerican journal of physiology. Heart and circulatory physiology · 2018
    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

5 authors at 2 institutions in 1 country.

Chun ZhouDepartment of Physiology and Cell Biology, University of South Alabama, Mobile, Alabama; Center for Lung Biology, University of South Alabama, Mobile, Alabama; and.
Mary I TownsleyDepartment of Physiology and Cell Biology, University of South Alabama, Mobile, Alabama; Department of Internal Medicine, University of South Alabama, Mobile, Alabama; Center for Lung Biology, University of South Alabama, Mobile, Alabama; and.
Mikhail AlexeyevDepartment of Physiology and Cell Biology, University of South Alabama, Mobile, Alabama; Center for Lung Biology, University of South Alabama, Mobile, Alabama; and.
Norbert F VoelkelDivision of Pulmonary Disease and Critical Care Medicine, Department of Internal Medicine, Virginia Commonwealth University, Richmond, Virginia.
Troy StevensDepartment of Physiology and Cell Biology, University of South Alabama, Mobile, Alabama; Department of Internal Medicine, University of South Alabama, Mobile, Alabama; Center for Lung Biology, University of South Alabama, Mobile, Alabama; and tstevens@southalabama.edu.
University of South Alabama · USVirginia Commonwealth University · US

Funding

Store-operated calcium entry: lung endothelial permeabilityR37HL060024 · NHLBI · UNIVERSITY OF SOUTH ALABAMA · PI STEVENS, TROY · 2010 to 2019
$3.9M
Mouse models for mitochondrial disorders caused by mutations in mtDNAR01OD010944 · OD · UNIVERSITY OF SOUTH ALABAMA · PI ALEXEYEV, MIKHAIL F., WALLACE, DOUGLAS C · 2012 to 2020
$2.6M
NHLBI NIH HHS R37 HL060024NIH HHS R01 OD010944
6 · The paper itself

Abstract

Here, we tested the hypothesis that animals with severe pulmonary arterial hypertension (PAH) display increased sensitivity to vascular permeability induced by activation of store-operated calcium entry. To test this hypothesis, wild-type and transient receptor potential channel 4 (TRPC4) knockout Fischer 344 rats were given a single injection of Semaxanib (SU5416; 20 mg/kg) followed by 3 wk of exposure to hypoxia (10% oxygen) and a return to normoxia (21% oxygen) for an additional 2-3 wk. This Semaxanib/hypoxia/normoxia (i.e., SU5416/hypoxia/normoxia) treatment caused PAH, as evidenced by development of right ventricular hypertrophy, pulmonary artery medial hypertrophy, and occlusive lesions within precapillary arterioles. Pulmonary artery pressure was increased fivefold in Semaxanib/hypoxia/normoxia-treated animals compared with untreated, Semaxanib-treated, and hypoxia-treated controls, determined by isolated perfused lung studies. Thapsigargin induced a dose-dependent increase in permeability that was dependent on TRPC4 in the normotensive perfused lung. This increase in permeability was accentuated in PAH lungs but not in Semaxanib- or hypoxia-treated lungs. Fluid accumulated in large perivascular cuffs, and although alveolar fluid accumulation was not seen in histological sections, Evans blue dye conjugated to albumin was present in bronchoalveolar lavage fluid of hypertensive but not normotensive lungs. Thus PAH is accompanied by a TRPC4-dependent increase in the sensitivity to edemagenic agents that activate store-operated calcium entry.

Indexed as

Calcium SignalingAnimalsArterial PressureCell HypoxiaEndothelium, VascularHypertension, PulmonaryIndolesMalePermeabilityPyrrolesRats, Inbred F344ThapsigarginTRPC Cation ChannelsIndolesPyrrolesSemaxinibThapsigarginTRPC4 ion channelTRPC Cation Channelscalcium channelscanonical transient receptor potential 4edemafiltration coefficientSemaxanibSugen 5416TRPC4

Identifiers

PMID27422996
PMCPMC5142214
OpenAlexW2473222548

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.