{"id":{"repo_id":"uwo","oai_identifier":"oai:uwo.scholaris.ca:20.500.14721/34178"},"canonical_url":"https://search.dev.ndltd.org/etd/uwo/oai:uwo.scholaris.ca:20.500.14721/34178","repository":{"repo_id":"uwo","name":"Western University","base_url":"https://uwo.scholaris.ca/server/oai/request"},"display":{"title":"The Long Non-coding RNA Malat1 Regulates Inflammatory Cytokine Production in Chronic Diabetic Complications","abstract":"We examined the role of MALAT1, a highly conserved nuclear lncRNA, in chronic diabetic complications affecting the heart and kidneys, specifically with respect to inflammatory cytokine production. Endothelial cells, exposed to various glucose levels, and MALAT1 knockout mice and controls, with or without streptozotocin-induced diabetes were examined. Endothelial cells cultured with high glucose, and renal and cardiac tissue from diabetic mice showed increased inflammatory cytokine (eg. IL-6, IL1β, TNFα) production along with transient MALAT1 upregulation. This was confirmed by both transcript and protein analyses, and such changes were prevented in the MALAT1 knockout diabetic animals. In the malat1 knockout animals, diabetes-induced cardiac dysfunction was also prevented. We further identified that such actions of MALAT1 are mediated by specific downstream molecules including SAA3 and p53. The data from this study provided direct evidence to the importance of MALAT1 in the pathogenesis of chronic diabetic complications involving the heart and kidneys.","abstract_html":"We examined the role of MALAT1, a highly conserved nuclear lncRNA, in chronic diabetic complications affecting the heart and kidneys, specifically with respect to inflammatory cytokine production. Endothelial cells, exposed to various glucose levels, and MALAT1 knockout mice and controls, with or without streptozotocin-induced diabetes were examined. Endothelial cells cultured with high glucose, and renal and cardiac tissue from diabetic mice showed increased inflammatory cytokine (eg. IL-6, IL1β, TNFα) production along with transient MALAT1 upregulation. This was confirmed by both transcript and protein analyses, and such changes were prevented in the MALAT1 knockout diabetic animals. In the malat1 knockout animals, diabetes-induced cardiac dysfunction was also prevented. We further identified that such actions of MALAT1 are mediated by specific downstream molecules including SAA3 and p53. The data from this study provided direct evidence to the importance of MALAT1 in the pathogenesis of chronic diabetic complications involving the heart and kidneys.","abstract_has_math":false,"creators":["Gordon, Andrew D"],"institution":"The University of Western Ontario","degree_name":"M Sc","degree_level":null,"degree_discipline":"Pathology","degree_department":null,"school":null,"contributors":[],"advisors":["Chakrabarti, Subrata"],"committee_chairs":[],"committee_members":[],"year":2016,"date_issued":"2016-09-09","date_published":"2016-09-09","updated_at":"2026-07-27T21:55:54Z","subjects":["MALAT1","LncRNA","Diabetes"],"languages":["en_ca"],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://hdl.handle.net/20.500.14721/34178","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Chakrabarti, Subrata"]},{"key":"dc:creator","label":"Author","values":["Gordon, Andrew D"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2025-07-10T20:00:32Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2025-07-10T20:00:32Z"]},{"key":"dc:date.issued","label":"Date","values":["2016-09-09"]},{"key":"dc:publisher","label":"Institution","values":["The University of Western Ontario"]},{"key":"dc:type","label":"Dc Type","values":["thesis"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Pathology"]},{"key":"thesis:degree_name","label":"Degree Name","values":["M Sc"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["MALAT1","LncRNA","Diabetes"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en_ca"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["https://hdl.handle.net/20.500.14721/34178"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["The thesis cover page in the PDF document includes references to Western University’s previous institutional repository platform, known as Scholarship@Western, and links to that platform (beginning with ir.lib.uwo.ca). In citing or referring to this thesis, use the DOI or handle from this page instead. Sample citation: Author name, \"Thesis title.\" (Year). Western University Open Repository. https://doi.org/10.71858/123456."]},{"key":"dc:description.abstract","label":"Abstract","values":["We examined the role of MALAT1, a highly conserved nuclear lncRNA, in chronic diabetic complications affecting the heart and kidneys, specifically with respect to inflammatory cytokine production. Endothelial cells, exposed to various glucose levels, and MALAT1 knockout mice and controls, with or without streptozotocin-induced diabetes were examined. Endothelial cells cultured with high glucose, and renal and cardiac tissue from diabetic mice showed increased inflammatory cytokine (eg. IL-6, IL1β, TNFα) production along with transient MALAT1 upregulation. This was confirmed by both transcript and protein analyses, and such changes were prevented in the MALAT1 knockout diabetic animals. In the malat1 knockout animals, diabetes-induced cardiac dysfunction was also prevented. We further identified that such actions of MALAT1 are mediated by specific downstream molecules including SAA3 and p53. The data from this study provided direct evidence to the importance of MALAT1 in the pathogenesis of chronic diabetic complications involving the heart and kidneys."]},{"key":"dc:title","label":"Title","values":["The Long Non-coding RNA Malat1 Regulates Inflammatory Cytokine Production in Chronic Diabetic Complications"]}]}],"canonical_facts":{"dc:contributor.advisor":["Chakrabarti, Subrata"],"dc:creator":["Gordon, Andrew D"],"dc:date.accessioned":["2025-07-10T20:00:32Z"],"dc:date.available":["2025-07-10T20:00:32Z"],"dc:date.issued":["2016-09-09"],"dc:description":["The thesis cover page in the PDF document includes references to Western University’s previous institutional repository platform, known as Scholarship@Western, and links to that platform (beginning with ir.lib.uwo.ca). In citing or referring to this thesis, use the DOI or handle from this page instead. Sample citation: Author name, \"Thesis title.\" (Year). Western University Open Repository. https://doi.org/10.71858/123456."],"dc:description.abstract":["We examined the role of MALAT1, a highly conserved nuclear lncRNA, in chronic diabetic complications affecting the heart and kidneys, specifically with respect to inflammatory cytokine production. Endothelial cells, exposed to various glucose levels, and MALAT1 knockout mice and controls, with or without streptozotocin-induced diabetes were examined. Endothelial cells cultured with high glucose, and renal and cardiac tissue from diabetic mice showed increased inflammatory cytokine (eg. IL-6, IL1β, TNFα) production along with transient MALAT1 upregulation. This was confirmed by both transcript and protein analyses, and such changes were prevented in the MALAT1 knockout diabetic animals. In the malat1 knockout animals, diabetes-induced cardiac dysfunction was also prevented. We further identified that such actions of MALAT1 are mediated by specific downstream molecules including SAA3 and p53. The data from this study provided direct evidence to the importance of MALAT1 in the pathogenesis of chronic diabetic complications involving the heart and kidneys."],"dc:identifier.uri":["https://hdl.handle.net/20.500.14721/34178"],"dc:language.iso":["en_ca"],"dc:publisher":["The University of Western Ontario"],"dc:subject":["MALAT1","LncRNA","Diabetes"],"dc:title":["The Long Non-coding RNA Malat1 Regulates Inflammatory Cytokine Production in Chronic Diabetic Complications"],"dc:type":["thesis"],"thesis:degree_discipline":["Pathology"],"thesis:degree_name":["M Sc"]},"updated_at":"2026-07-27T21:55:54Z"}