Evidence map›Paper›PMID 21890695›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2011

The Rho kinase inhibitor Y-27632 increases erythrocyte deformability and low oxygen tension-induced ATP release.

K M Thuet, E A Bowles, M L Ellsworth, R S Sprague, A H Stephenson

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Myosin IIA interacts with the spectrin-actin membrane skeleton to control red blood cell membrane curvature and deformability.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  8. Review
  9. Review
  10. The functional significance of the rho/rho-kinase pathway in human erythrocytes.Turkish journal of haematology : official journal of Turkish Society of Haematology · 2014
    Article
  11. Rho-kinase inhibition improves ischemic perfusion deficit in hyperlipidemic mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2014
    Article
  12. Article
  13. 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 1 institution in 1 country.

K M ThuetDepartment of Pharmacological and Physiological Science, St. Louis University School of Medicine, St. Louis, MO 63104, USA. thuetk@slu.edu
E A Bowles
M L Ellsworth
R S Sprague
A H Stephenson
Saint Louis University · US

Funding

MECHANISMS OF DEFORMATION-INDUCED ATP RELEASE FROM RBCSR01HL064180 · NHLBI · SAINT LOUIS UNIVERSITY · PI SPRAGUE, RANDY · 2000 to 2007
$2.3M
Microvascular O2 Delivery: Impact of Erythrocyte-Released ATPR33HL089094 · NHLBI · SAINT LOUIS UNIVERSITY · PI ELLSWORTH, MARY L · 2007 to 2009
$1.6M
NHLBI NIH HHS HL-64180NHLBI NIH HHS HL-89094
6 · The paper itself

Abstract

Low oxygen (O(2)) tension and mechanical deformation are stimuli for ATP release from erythrocytes. It has been shown previously that rabbit erythrocytes made less deformable with diamide, a thiol cross-linking agent, release less ATP in response to low O(2) tension, suggesting a link between these two stimuli. In nonerythroid cells, activation of the Rho/Rho kinase signaling pathway has been reported to decrease cell deformability by altering Rho kinase-dependent cytoskeleton-protein interactions. We investigated the hypothesis that the Rho kinase inhibitor Y-27632 would increase erythrocyte deformability and thereby increase low O(2) tension-induced ATP release from erythrocytes. Here we show that Y-27632 (1 μM) increases erythrocyte deformability (5%) and increases low O(2) tension-induced ATP release (203%) from healthy human erythrocytes. In addition, we found that, when erythrocytes were made less deformable by incubation with diamide (100 μM), Y-27632 restored both deformability and low O(2) tension-induced ATP release to levels similar to those measured in the absence of diamide. These findings suggest that the Rho kinase inhibitor Y-27632 is able to reverse the diamide-induced decrease in erythrocyte deformability and rescue low O(2) tension-induced ATP release. These results further support a link between erythrocyte deformability and ATP release in response to low O(2) tension.

Indexed as

Adenosine TriphosphateAmidesCell HypoxiaCross-Linking ReagentsDiamideErythrocyte DeformabilityErythrocytesHumansIntercellular Signaling Peptides and ProteinsOxygenPeptidesProtein Kinase InhibitorsPyridinesrhoA GTP-Binding Proteinrho-Associated KinasesSulfhydryl ReagentsAdenosine TriphosphateAmidesCross-Linking ReagentsDiamideIntercellular Signaling Peptides and ProteinsmastoparanOxygenPeptidesProtein Kinase InhibitorsPyridinesrhoA GTP-Binding ProteinRHOA protein, humanrho-Associated KinasesSulfhydryl ReagentsWasp VenomsY 27632

Identifiers

PMID21890695
PMCPMC3213963
OpenAlexW2105402035

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.