Effect of Molecular and Cellular Blood Composition on the Kinetics of Clot Contraction

Monday, May 9, 2016

11:00 AM-1:00 PM

BIOMED PhD Research Proposal

Speaker:
Valerie Tutwiler, PhD Candidate, School of Biomedical Engineering, Science and Health Systems

Advisors:
Kara Spiller, PhD, Assistant Professor, School of Biomedical Engineering, Science and Health Systems; and John Weisel, PhD, Professor of Cell and Developmental Biology, University of Pennsylvania

Title:
Effect of Molecular and Cellular Blood Composition on the Kinetics of Clot Contraction

Abstract:
Venous thromboembolism, myocardial infarction and stroke lead in causes of death and disability worldwide. Clot contraction, which is the platelet-driven reduction of the clot volume, has been implicated to play a critical role in preventing blood loss and restoring blood flow past otherwise obstructive thrombi. Clot composition varies based on the origin of the clot, with thrombi formed in the veins having a substantial portion of thrombus volume made of red blood cells (RBCs). Despite the implied importance of clot contraction, the gaps in our understanding can be, in part, attributed to previous lack of methodology to quantify the dynamic process.

Through the use of a novel optical tracking methodology we aim to 1) assess the effect of the cellular and molecular composition of the blood on the time course of clot contraction, 2) study mechanistic differences between clot contraction in healthy donors and patients with pathological conditions such as sickle cell disease and ischemic stroke, particularly the modulation of RBC deformability, and 3) quantify how clot contraction affects the sensitivity to fibrinolytic agents such as tissue-type plasminogen activator. Optical tracking will be combined with high precision rheometry, scanning electron microscopy, and an active viscoelastic model to describe clot contraction and predict how pathological changes in the blood composition affect clot contraction.

This quantitative study of clot contraction in healthy and pathological conditions will advance the understanding of the mechanism(s) of clot contraction and potentially inform the development of more effective and timely treatments to promote hemostasis, limit thrombosis and control bleeding.

Contact Information

Ken Barbee
215-895-1335
barbee@drexel.edu