{"id":{"repo_id":"wfu","oai_identifier":"oai:wakespace.lib.wfu.edu:10339/37294"},"canonical_url":"https://search.dev.ndltd.org/etd/wfu/oai:wakespace.lib.wfu.edu:10339/37294","repository":{"repo_id":"wfu","name":"Wake Forest University","base_url":"https://wakespace.lib.wfu.edu/oai/request"},"display":{"title":"The Role of ACAT2 in the Initiation and Treatment of Atherosclerosis","abstract":"Hepatic acyl coenzyme A:cholesterol acyltransferase 2 (ACAT2) synthesizes cholesteryl ester (CE) from free cholesterol and fatty acyl-CoA. ACAT2 is responsible for the packaging of cholesteryl oleate (CO) into VLDL secreted from the liver and studies have shown a relationship between both ACAT2 activity and CO content of apoB-containing lipoproteins with atherosclerosis. The purpose of the studies was to extend our understanding of ACAT2 and primarily to elucidate its role in the initiation and treatment of atherosclerosis. To elucidate it's role in the initiation of atherosclerosis we proposed that as a result of elevated ACAT2 activity, more CO would be packaged into the low-density lipoprotein (LDL) core and resulting in a particle with a greater likelihood to be retained in the artery wall. To determine it's role in the treatment of atherosclerosis, we utilized an antisense oligonucleotide (ASO) to knockdown ACAT2 expression in the liver to determine how depleting atherogenic particles of CO would effect atherosclerotic lesion regression.","abstract_html":"Hepatic acyl coenzyme A:cholesterol acyltransferase 2 (ACAT2) synthesizes cholesteryl ester (CE) from free cholesterol and fatty acyl-CoA. ACAT2 is responsible for the packaging of cholesteryl oleate (CO) into VLDL secreted from the liver and studies have shown a relationship between both ACAT2 activity and CO content of apoB-containing lipoproteins with atherosclerosis. The purpose of the studies was to extend our understanding of ACAT2 and primarily to elucidate its role in the initiation and treatment of atherosclerosis. To elucidate it's role in the initiation of atherosclerosis we proposed that as a result of elevated ACAT2 activity, more CO would be packaged into the low-density lipoprotein (LDL) core and resulting in a particle with a greater likelihood to be retained in the artery wall. To determine it's role in the treatment of atherosclerosis, we utilized an antisense oligonucleotide (ASO) to knockdown ACAT2 expression in the liver to determine how depleting atherogenic particles of CO would effect atherosclerotic lesion regression.","abstract_has_math":false,"creators":["Melchior, John Trevvett"],"institution":"Wake Forest University","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2012,"date_issued":"2012","date_published":"2012","updated_at":"2026-07-27T22:01:27Z","subjects":["ACAT2"],"languages":["en"],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/10339/37294","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Melchior, John Trevvett"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2012-06-12T08:36:02Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2012-12-12T09:30:07Z"]},{"key":"dc:date.issued","label":"Date","values":["2012"]},{"key":"dc:publisher","label":"Institution","values":["Wake Forest University"]},{"key":"dc:type","label":"Dc Type","values":["Dissertation"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["ACAT2"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/10339/37294"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Hepatic acyl coenzyme A:cholesterol acyltransferase 2 (ACAT2) synthesizes cholesteryl ester (CE) from free cholesterol and fatty acyl-CoA. ACAT2 is responsible for the packaging of cholesteryl oleate (CO) into VLDL secreted from the liver and studies have shown a relationship between both ACAT2 activity and CO content of apoB-containing lipoproteins with atherosclerosis. The purpose of the studies was to extend our understanding of ACAT2 and primarily to elucidate its role in the initiation and treatment of atherosclerosis. To elucidate it's role in the initiation of atherosclerosis we proposed that as a result of elevated ACAT2 activity, more CO would be packaged into the low-density lipoprotein (LDL) core and resulting in a particle with a greater likelihood to be retained in the artery wall. To determine it's role in the treatment of atherosclerosis, we utilized an antisense oligonucleotide (ASO) to knockdown ACAT2 expression in the liver to determine how depleting atherogenic particles of CO would effect atherosclerotic lesion regression."]},{"key":"dc:title","label":"Title","values":["The Role of ACAT2 in the Initiation and Treatment of Atherosclerosis"]}]}],"canonical_facts":{"dc:creator":["Melchior, John Trevvett"],"dc:date.accessioned":["2012-06-12T08:36:02Z"],"dc:date.available":["2012-12-12T09:30:07Z"],"dc:date.issued":["2012"],"dc:description.abstract":["Hepatic acyl coenzyme A:cholesterol acyltransferase 2 (ACAT2) synthesizes cholesteryl ester (CE) from free cholesterol and fatty acyl-CoA. ACAT2 is responsible for the packaging of cholesteryl oleate (CO) into VLDL secreted from the liver and studies have shown a relationship between both ACAT2 activity and CO content of apoB-containing lipoproteins with atherosclerosis. The purpose of the studies was to extend our understanding of ACAT2 and primarily to elucidate its role in the initiation and treatment of atherosclerosis. To elucidate it's role in the initiation of atherosclerosis we proposed that as a result of elevated ACAT2 activity, more CO would be packaged into the low-density lipoprotein (LDL) core and resulting in a particle with a greater likelihood to be retained in the artery wall. To determine it's role in the treatment of atherosclerosis, we utilized an antisense oligonucleotide (ASO) to knockdown ACAT2 expression in the liver to determine how depleting atherogenic particles of CO would effect atherosclerotic lesion regression."],"dc:identifier.uri":["http://hdl.handle.net/10339/37294"],"dc:language.iso":["en"],"dc:publisher":["Wake Forest University"],"dc:subject":["ACAT2"],"dc:title":["The Role of ACAT2 in the Initiation and Treatment of Atherosclerosis"],"dc:type":["Dissertation"]},"updated_at":"2026-07-27T22:01:27Z"}