2026-09-19T16:36:49Zhttps://ecommons.cornell.edu/server/oai/requestoai:ecommons.cornell.edu:1813/371282026-05-14T13:51:41Zcom_1813_35col_1813_47
Sinha, Siddhartha
Leifer, Cynthia Anne
Weiss, Robert S.
Roberson, Mark Stephen
2014-07-28T19:25:04Z
2019-05-26T06:00:31Z
2014-05-25
https://hdl.handle.net/1813/37128
8641234
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.
en_US
Atherosclerosis
Inflammation
Macrophage
Role Of Substrate Stiffness In Driving Atherogenic Behavior In Macrophages.
dissertation or thesis
application/pdf
Physiology
Cornell University
Master of Science
M.S., Physiology
Publication
Cornell Theses and Dissertations
Sinha, Siddhartha
5893a6ea-7af3-41d7-abc6-04bcd26ab5df
open.access
open.access
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<Keyword>Atherosclerosis</Keyword>
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<Abstract>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.</Abstract>
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