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Platelet Interactions with the Blood Vessel Wall

Vascular Control of Platelets

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Platelets in Thrombotic and Non-Thrombotic Disorders

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Abstract

Appropriate hemostasis hinges on normal vascular control of platelet function to suppress thrombosis in the absence of blood vessel injury. In this regard, normal intercellular communication between vascular endothelial cells and platelets is integral to maintaining platelets in an inactivated state and inhibiting maladaptive clot (thrombus) formation. Conversely, disruption to endogenous synthesis of nitric oxide, prostaglandin I2, and endothelial cell surface-associated ecto-ADPase/CD39 occurring due to genetic or acquired factors is an important contributor to the pathogenesis of clinically important thrombotic pathophenotypes, including myocardial infarction and stroke. By analyzing differences in vascular control of platelets according to circulatory bed, particularly with respect to the pulmonary and systemic circuits, understanding the relevance of hypoxia, inflammation, blood flow, and oxidant stress to platelet aggregation and adhesion is enhanced. It is also anticipated that clarifying the biophysical and molecular sequence of events underpinning endothelial regulation of platelet activation will require next-generation methods that utilize whole organ platforms in silico to identify novel mediators of thrombosis in vivo and prevent the attendant adverse consequences in patients.

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Abbreviations

AC:

Adenylyl cyclase

ADP:

Adenosine diphosphate

ATP:

Adenosine triphosphate

CAD:

Coronary artery disease

cAMP:

Cyclic adenosine monophosphate

cGMP:

Cyclic guanosine monophosphate

COX:

Cyclooxygenase

CTEPH:

Chronic thromboembolic pulmonary hypertension

Da:

Dalton

H2O2 :

Hydrogen peroxide

IL:

Interleukin

IP3:

Inositol triphosphate

MLC:

Myosin light chain

MLCK:

Myosin light chain kinase

NO· :

Nitric oxide

\( {\mathrm{NO}}_2^{-} \) :

Nitrite

\( {\mathrm{NO}}_3^{-} \) :

Nitrate

NOS:

Nitric oxide synthase

NOx:

Nitrogen oxides

NOX:

NADPH oxidase

\( {\mathrm{O}}_2^{-\cdot } \) :

Superoxide anion

ONOO− :

Peroxynitrite

PAH:

Pulmonary arterial hypertension

PAI-1:

Plasminogen activator inhibitor-1

PG:

Prostaglandin

PKG:

Protein kinase G

ROS:

Reactive oxygen species

TXA:

Thromboxane A2

VWF:

Von Willebrand factor

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Acknowledgements

The authors wish to thank Ms. Stephanie Tribuna for expert technical assistance in the preparation of this manuscript.

Funding Sources NIH 1K08HL11207-01A1, AHA 15GRNT25080016, Pulmonary Hypertension Association, Cardiovascular Medical Research and Education Fund (CMREF), and Klarman Foundation (Brigham and Women’s Hospital) to B.A.M., and NIH grants HL048743, HL61795, HL108630, and GM107618 to J.L.

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Authors and Affiliations

  1. Cardiovascular Division, Department of Medicine, Harvard Medical School, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA, 02115, USA

    Bradley A. Maron M.D. & Joseph Loscalzo M.D., Ph.D.

  2. Department of Cardiology, Veterans Affairs Boston Healthcare System, West Roxbury, MA, 02132, USA

    Bradley A. Maron M.D.

Authors
  1. Bradley A. Maron M.D.
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  2. Joseph Loscalzo M.D., Ph.D.
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Correspondence to Joseph Loscalzo M.D., Ph.D. .

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Editors and Affiliations

  1. Department of Medicine, Section of Internal and Cardiovascular Medicine, University of Perugia , Perugia, Italy

    Paolo Gresele

  2. Houston Methodist Hospital , Houston, Texas, USA

    Neal S. Kleiman

  3. Bloodworks Northwest, University of Washington , Seattle, Washington, USA

    José A. Lopez

  4. Sackler Inst of Pulmonary Pharmacol, King’s College London, London, United Kingdom

    Clive P. Page

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Maron, B.A., Loscalzo, J. (2017). Platelet Interactions with the Blood Vessel Wall. In: Gresele, P., Kleiman, N., Lopez, J., Page, C. (eds) Platelets in Thrombotic and Non-Thrombotic Disorders. Springer, Cham. https://doi.org/10.1007/978-3-319-47462-5_29

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