Evidence map›Paper›PMID 30972780›Full record

ArticleArtificial organs2019

The role of PI3K/Akt signaling pathway in non-physiological shear stress-induced platelet activation.

Zengsheng Chen, Tieluo Li, Kafayat Kareem, Douglas Tran, Bartley P Griffith, Zhongjun J Wu

Open access · greenAbstract read
In one paragraph

Article in Artificial organs, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
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  10. Antiplatelet Effects of a Combination of Sappan Wood (Advances in pharmacological and pharmaceutical sciences · 2024
    Article
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  12. Review
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  16. Gegen Qinlian pills alleviate carrageenan-induced thrombosis in mice model by regulating the HMGB1/NF-κB/NLRP3 signaling.Phytomedicine : international journal of phytotherapy and phytopharmacology · 2022
    Article
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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.

Zengsheng ChenDepartment of Surgery, University of Maryland School of Medicine, Baltimore, Maryland.
Tieluo LiDepartment of Surgery, University of Maryland School of Medicine, Baltimore, Maryland.
Kafayat KareemDepartment of Surgery, University of Maryland School of Medicine, Baltimore, Maryland.
Douglas TranDepartment of Surgery, University of Maryland School of Medicine, Baltimore, Maryland.
Bartley P GriffithDepartment of Surgery, University of Maryland School of Medicine, Baltimore, Maryland.
Zhongjun J WuDepartment of Surgery, University of Maryland School of Medicine, Baltimore, Maryland.ORCID https://orcid.org/0000-0003-0807-7195
University of Maryland, Baltimore · US

Funding

Shear-Induced Hemostatic Dysfunction and Bleeding in CF-VAD PatientsR01HL124170 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI GRIFFITH, BARTLEY P, WU, ZHONGJUN JON · 2015 to 2018
$2.0M
NHLBI NIH HHS R01 HL124170NIH HHS R01HL124170.
6 · The paper itself

Abstract

The PI3K/Akt signaling pathway has been implicated in playing an important role in platelet activation during hemostasis and thrombosis involving platelet-matrix interaction and platelet aggregation. Its role in non-physiological shear stress (NPSS)-induced platelet activation relevant to high-shear blood contacting medical devices (BCMDs) is unclear. In the context of blood cells flowing in BCMDs, platelets are subjected to NPSS (>100 Pa) with very short exposure time (<1 s). In this study, we investigated whether NPSS with short exposure time induces platelet activation through the PI3K/Akt signaling pathway. Healthy donor blood treated with or without PI3K inhibitor was subjected to NPSS (150 Pa) with short exposure time (0.5 s). Platelet activation indicated by the surface P-selectin expression and activated glycoprotein (GP) IIb/IIIa was quantified using flow cytometry. The phosphorylation of Akt, activation of the PI3K signaling, was characterized by western blotting. Changes in adhesion behavior of NPSS-sheared platelets on fibrinogen, collagen, and von Willebrand factor (vWF) were quantified with fluorescent microscopy by perfusing the NPSS-sheared and PI3K inhibitor-treated blood through fibrinogen, collagen, and vWF-coated microcapillary tubes. The results showed that the PI3K/Akt signaling was involved with both NPSS-induced platelet activation and platelet-matrix interaction. NPSS-sheared platelets exhibited exacerbated platelet adhesion on fibrinogen, but had diminished platelet adhesion on collagen and vWF. The inhibition of PI3K signaling reduced P-selectin expression and GPIIb/IIIa activation with suppressed Akt phosphorylation and abolished NPSS-enhanced platelet adhesion on fibrinogen in NPSS-sheared blood. The inhibition of PI3K signaling can attenuate the adhesion of unsheared platelets (baseline) on collagen and vWF, while had no impact on adhesion of NPSS-sheared platelets on collagen and vWF. This study confirmed the important role of PI3K/Akt signaling pathway in NPSS-induced platelet activation. The finding of this study suggests that blocking PI3K/Akt signaling pathway could be a potential method to treat thrombosis in patients implanted with BCMDs.

Indexed as

Platelet ActivationSignal TransductionAdultBlood PlateletsFemaleHumansMalePhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktStress, MechanicalYoung AdultPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAkt phosphorylationblood contacting medical devicenon-physiological shear stressPI3K/Akt signaling pathwayplatelet activation

Identifiers

PMID30972780
PMCPMC6733652
OpenAlexW2937486782

What OpenQuestion holds

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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.