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dc.contributor.authorSinha, Siddharthaen_US
dc.date.accessioned2014-07-28T19:25:04Z
dc.date.available2019-05-26T06:00:31Z
dc.date.issued2014-05-25en_US
dc.identifier.otherbibid: 8641234
dc.identifier.urihttps://hdl.handle.net/1813/37128
dc.description.abstractAtherosclerosis 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
dc.language.isoen_USen_US
dc.subjectAtherosclerosisen_US
dc.subjectInflammationen_US
dc.subjectMacrophageen_US
dc.titleRole Of Substrate Stiffness In Driving Atherogenic Behavior In Macrophages.en_US
dc.typedissertation or thesisen_US
thesis.degree.disciplinePhysiology
thesis.degree.grantorCornell Universityen_US
thesis.degree.levelMaster of Science
thesis.degree.nameM.S., Physiology
dc.contributor.chairLeifer, Cynthia Anneen_US
dc.contributor.committeeMemberWeiss, Robert S.en_US
dc.contributor.committeeMemberRoberson, Mark Stephenen_US


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