Role Of Substrate Stiffness In Driving Atherogenic Behavior In Macrophages.

Atherosclerosis is a decades-long process whose patients often remain asymptomatic until after a heart attack or stroke. Novel therapeutic approaches focus on tuning the body's own atheroprotective mechanisms to induce regression. My approach looks at macrophages, which is the most prominent immune cell type in atherosclerotic plaque due to its involvement in lipid clearance, apoptotic cell debris clearance and pro- or anti-inflammatory cytokine production. While the molecular mechanisms active in lesional macrophages have been extensively studied, the effect of age- and inflammation-induced arterial stiffening on macrophage function is not yet fully understood. Thanks to recent advances in bioengineering that provided the tools to mimic physical properties of tissue, the effect of physical stiffness and associated matrix remodeling on macrophages can now be studied. Herein I describe the effects of physical substrate stiffness on macrophage behavior relevant to atherosclerosis plaque formation using a polyacrylamide hydrogel-based in vitro model of atherosclerotic tissue.

Name thesis:degree_name

M.S., Physiology

Level thesis:degree_level

Master of Science

Discipline thesis:degree_discipline

Physiology

Grantor

Cornell University

Year dc:date.issued

2014

Author dc:creator

• Sinha, Siddhartha

Committee members dc:contributor.committeemember

• Weiss, Robert S.
• Roberson, Mark Stephen

• Atherosclerosis
• Inflammation
• Macrophage

Language dc:language.iso

en_US

Handle dc:identifier.uri

https://hdl.handle.net/1813/37128

OAI identifier oai:identifier

oai:ecommons.cornell.edu:1813/37128