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Related Experiment Video

Updated: Nov 6, 2025

A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry
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mTOR regulates GPVI-mediated platelet activation.

Longsheng Wang1, Gang Liu1,2, Nannan Wu1

  • 1Chronic Disease Research Institute, Department of Nutrition and Food Hygiene, Zhejiang University School of Public Health, 866 Yu-Hang-Tang Road, Hangzhou, 310058, China.

Journal of Translational Medicine
|May 11, 2021
PubMed
Summary
This summary is machine-generated.

Mammalian target of rapamycin (mTOR) is crucial for platelet activation and thrombus formation, particularly in response to low-dose agonists. Its absence impairs platelet aggregation and dense granule secretion, highlighting mTOR

Keywords:
Dense granule secretion (ATP release)GPVIPkcδPlateletsmTOR

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Area of Science:

  • Hematology
  • Molecular Biology
  • Biochemistry

Background:

  • Mammalian target of rapamycin (mTOR) gene-loss in mice causes embryonic lethality, preventing direct study of mTOR's role in platelets via knockout.
  • Previous research has not fully elucidated the function of mTOR in platelet activation and thrombus formation due to genetic limitations.

Purpose of the Study:

  • To investigate the role of mTOR in platelet activation and thrombus formation using a novel megakaryocyte/platelet-specific mTOR knockout mouse model.
  • To determine the impact of mTOR deletion on platelet aggregation, dense granule secretion, and in vivo thrombosis.

Main Methods:

  • Generation of a mouse model with megakaryocyte/platelet-specific deletion of mTOR.
  • Evaluation of thrombus formation in vitro using low and high concentration collagen-coated surfaces.
  • Assessment of FeCl3-induced mesenteric arteriole thrombosis in vivo.
  • Analysis of platelet aggregation, dense granule secretion (ATP release), and αIIbβ3 activation in response to various agonists.
  • Investigation of signaling pathways, including S6K1, S6, Akt, and PKC phosphorylation, in mTOR-deficient platelets.

Main Results:

  • mTOR-deficient platelets showed impaired thrombus formation on low-concentration collagen but not on high-concentration surfaces.
  • In vivo thrombosis models revealed significantly different responses in mTOR-deficient mice to low-extent injury.
  • Reduced platelet aggregation and ATP release were observed in response to low doses of GPVI and PAR4 agonists, with dose-dependent recovery.
  • Low-dose agonist stimulation of mTOR-deficient platelets resulted in decreased αIIbβ3 activation and altered phosphorylation of key signaling molecules (S6K1, S6, Akt, PKCδ, PKCε).

Conclusions:

  • mTOR plays a critical role in glycoprotein VI (GPVI)-dependent platelet activation and thrombus formation.
  • The findings suggest a dose-dependent involvement of mTOR in platelet function, particularly under conditions of low agonist stimulation.
  • PKCδ and PKCε, especially PKCδ, are implicated in low-dose GPVI-mediated and mTOR-dependent platelet signaling.