Evidence map›Paper›PMID 27548633›Full record

ArticleJournal of biomechanical engineering2016

Nonmuscle Myosin IIA Regulates Platelet Contractile Forces Through Rho Kinase and Myosin Light-Chain Kinase.

Shirin Feghhi, Wes W Tooley, Nathan J Sniadecki

Open access · bronzeAbstract read
In one paragraph

Article in Journal of biomechanical engineering, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

18 citing papers in PubMed, 36 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Molecular Mechanisms Linking Diabetes with Increased Risk of Thrombosis.International journal of molecular sciences · 2023
    Review
  6. Blood clot contraction: Mechanisms, pathophysiology, and disease.Research and practice in thrombosis and haemostasis · 2023
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. A Novel Platelet Function Assay for Trauma.The Journal of surgical research · 2020
    Observational
  13. Article
  14. Review
  15. Article
  16. Article
  17. Observational
  18. A Useful Device to Measure Kinetics of Platelet Contraction.ASAIO journal (American Society for Artificial Internal Organs : 1992)
    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

3 authors at 1 institution in 1 country.

Shirin Feghhi
Wes W Tooley
Nathan J Sniadecki
University of Washington · US

Funding

Bioengineering Cardiovascular Training GrantT32EB001650 · NIBIB · UNIVERSITY OF WASHINGTON · PI REGNIER, MICHAEL · 2004 to 2019
$3.6M
Subcellular Platelet Forces and AdhesionsR21HL097284 · NHLBI · UNIVERSITY OF WASHINGTON · PI SNIADECKI, NATHAN JOHN · 2009 to 2010
$394k
NHLBI NIH HHS R21 HL097284NIBIB NIH HHS T32 EB001650
6 · The paper itself

Abstract

Platelet contractile forces play a major role in clot retraction and help to hold hemostatic clots against the vessel wall. Platelet forces are produced by its cytoskeleton, which is composed of actin and nonmuscle myosin filaments. In this work, we studied the role of Rho kinase, myosin light-chain kinase, and myosin in the generation of contractile forces by using pharmacological inhibitors and arrays of flexible microposts to measure platelet forces. When platelets were seeded onto microposts, they formed aggregates on the tips of the microposts. Forces produced by the platelets in the aggregates were measured by quantifying the deflection of the microposts, which bent in proportion to the force of the platelets. Platelets were treated with small molecule inhibitors of myosin activity: Y-27632 to inhibit the Rho kinase (ROCK), ML-7 to inhibit myosin light-chain kinase (MLCK), and blebbistatin to inhibit myosin ATPase activity. ROCK inhibition reduced platelet forces, demonstrating the importance of the assembly of actin and myosin phosphorylation in generating contractile forces. Similarly, MLCK inhibition caused weaker platelet forces, which verifies that myosin phosphorylation is needed for force generation in platelets. Platelets treated with blebbistatin also had weaker forces, which indicates that myosin's ATPase activity is necessary for platelet forces. Our studies demonstrate that myosin ATPase activity and the regulation of actin-myosin assembly by ROCK and MLCK are needed for the generation of platelet forces. Our findings illustrate and explain the importance of myosin for clot compaction in hemostasis and thrombosis.

Indexed as

Blood PlateletsCells, CulturedCytoskeletonHemostasisHumansMyosin-Light-Chain KinaseNonmuscle Myosin Type IIAPlatelet Aggregationrho-Associated KinasesStress, MechanicalMyosin-Light-Chain KinaseNonmuscle Myosin Type IIArho-Associated Kinases

Identifiers

PMID27548633
PMCPMC5013426
OpenAlexW2513564240

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.