@article{73fd66827d054371aaa4f6f7b10c9183,
title = "Is the endothelial cell responsible for the thrombus core and shell architecture?",
abstract = "Ischemia leading to heart attacks and strokes is the major cause of deaths in the world. This report explores the possibility that intracellular material from ruptured endothelial cells is partially responsible for the heterogeneous core-and-shell blood clot architecture, typically observed using intravital microscopy. As evidence, we present a fluid dynamic argument that platelet agonists emanating from the injury cannot activate platelets in the thrombus core, given that they would have to travel against flow of blood escaping into the extravascular. Furthermore, we demonstrate visual evidence that the core material appears to be continuous and originating from the damaged endothelium. Finally, we present a mechanism, illustrating the steps of platelet recruitment into the thrombus and sealing of the injury. If correct, the model presented herein will be beneficial to the understanding and treatment of heart attacks, strokes and hemophilia.",
keywords = "Core, Endothelial cells, P-selectin, Platelet activation, Platelets, Shell, Thrombogenesis",
author = "Kadri, {Olufemi Emmanuel} and Migle Surblyte and Chandran, {Vishnu Deep} and Voronov, {Roman S.}",
note = "Funding Information: We would like to thank the Prof. Skip Brass laboratory (including Prof. Timothy J. Stalker and Dr. John D. Welsh)at the University of Pennsylvania's Perelman School of Medicine for performing all the experiments and sharing their microscopy data. Also, we acknowledge that a part of this work was initiated under the guidance of Prof. Scott L. Diamond at the University of Pennsylvania Department of Chemical and Biomolecular Engineering, and Bioengineering Institute for Medicine & Engineering. The study was financially supported by the New Jersey Health Foundation Grant #PC101-17, and in part by NIH R01-HL103419 “Blood Systems Biology” grant and AHA 11POST6890012 Postdoctoral Fellowship. Undergraduate labor was supported by Shodor's Blue Waters 2018-2019 Student Internship Program. Funding Information: We would like to thank the Prof. Skip Brass laboratory (including Prof. Timothy J. Stalker and Dr. John D. Welsh) at the University of Pennsylvania{\textquoteright}s Perelman School of Medicine for performing all the experiments and sharing their microscopy data. Also, we acknowledge that a part of this work was initiated under the guidance of Prof. Scott L. Diamond at the University of Pennsylvania Department of Chemical and Biomolecular Engineering, and Bioengineering Institute for Medicine & Engineering. The study was financially supported by the New Jersey Health Foundation Grant #PC101-17, and in part by NIH R01-HL103419 “Blood Systems Biology” grant and AHA 11POST6890012 Postdoctoral Fellowship. Undergraduate labor was supported by Shodor{\textquoteright}s Blue Waters 2018-2019 Student Internship Program. Publisher Copyright: {\textcopyright} 2019 Elsevier Ltd",
year = "2019",
month = aug,
doi = "10.1016/j.mehy.2019.109244",
language = "English (US)",
volume = "129",
journal = "Medical Hypotheses",
issn = "0306-9877",
publisher = "Churchill Livingstone",
}