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Author Notes:

Email Address: yongzhi.qiu@emory.edu

Conceived and designed the experiments: MFK WAL YQ. Performed the experiments: MFK DRM YS YQ.

Analyzed the data: MFK WAL YQ. Wrote the paper: MFK WAL YQ.

The funders had no role in study design, data collection and analysis decision to publish, or preparation of the manuscript.

Co-author Wilbur Lam is a PLOS ONE Editorial Board member. This does not alter the authors' adherence to PLOS ONE Editorial policies and criteria.


Research Funding:

National Science Foundation CAREER Award 1150235 (to W.A.L.)

American Heart Association Innovative Research Grant (to W.A.L.)

National Institutes of Health grants U54HL112309 (to W.A.L.) and R01HL121264 (to W.A.L.)

American Heart Association Postdoctoral Fellowships (to D.R.M.).


  • Science & Technology
  • Multidisciplinary Sciences
  • Science & Technology - Other Topics
  • GPVI
  • CELL

Platelet Mechanosensing of Collagen Matrices


Journal Title:



Volume 10, Number 4


, Pages e0126624-e0126624

Type of Work:

Article | Final Publisher PDF


During vascular injury, platelets adhere to exposed subendothelial proteins, such as collagen, on the blood vessel walls to trigger clot formation. Although the biochemical signalings of platelet-collagen interactions have been well characterized, little is known about the role microenvironmental biomechanical properties, such as vascular wall stiffness, may have on clot formation. To that end, we investigated how substrates of varying stiffness conjugated with the same concentration of Type I collagen affect platelet adhesion, spreading, and activation. Using collagen-conjugated polyacrylamide (PA) gels of different stiffnesses, we observed that platelets do in fact mechanotransduce the stiffness cues of collagen substrates, manifesting in increased platelet spreading on stiffer substrates. In addition, increasing substrate stiffness also increases phosphatidylserine exposure, a key aspect of platelet activation that initiates coagulation on the platelet surface. Mechanistically, these collagen substrate stiffness effects are mediated by extracellular calcium levels and actomyosin pathways driven by myosin light chain kinase but not Rho-associated protein kinase. Overall, our results improve our understanding of how the mechanics of different tissues and stroma affect clot formation, what role the increased vessel wall stiffness in atherosclerosis may directly have on thrombosis leading to heart attacks and strokes, and how age-related increased vessel wall stiffness affects hemostasis and thrombosis.

Copyright information:

© 2015 Kee et al.

This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits distribution, public display, and publicly performance, making multiple copies, distribution of derivative works, provided the original work is properly cited. This license requires credit be given to copyright holder and/or author, copyright and license notices be kept intact.

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