Bioactive oxidized phosphatidylcholines cause apoptotic cell death in cardiomyocytes during ischemia reperfusion

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dc.contributor.authorHasanally, Devin
dc.contributor.examiningcommitteeJassal, Davinder S. (Physiology and Pathophysiology) Dixon, Ian M. C. (Physiology and Pathophysiology) Wigle, Jeffrey (Biochemistry and Medical Genetics)en_US
dc.contributor.supervisorRavandi, Amir (Physiology and Pathophysiology) Kirshenbaum, Lorrie A. (Physiology and Pathophysiology)en_US
dc.date.accessioned2015-04-08T20:59:56Z
dc.date.available2015-04-08T20:59:56Z
dc.date.issued2014en_US
dc.degree.disciplinePhysiology and Pathophysiologyen_US
dc.degree.levelMaster of Science (M.Sc.)en_US
dc.description.abstractThe main treatment for myocardial infarction is early reperfusion of ischemic tissue. Ischemia and reperfusion (IR) produces reactive oxygen species that oxidize membrane phospholipids. The production of oxidized lipids and their role on cell death in cardiac IR injury is unknown. Using in vitro model of IR, our goal was to identify oxidized phosphatidylcholines (OxPC) from cardiomyocytes, to determine their bioactivity on cardiomyocyte viability and mitochondrial permeability, and using an OxPC specific EO6 antibody inhibit OxPC activity on cardiomyocytes. Rat cardiomyocytes were exposed to IR and lipid extracts underwent lipidomic analysis with HPLC-MS/MS to quantitate 82 novel OxPC species. Cell viability and mitochondrial permeability were determined in vehicle control, non-oxidized control PC, and fragmented OxPC molecules. EO6 antibody was applied and cell viability was assessed. Cardiomyocytes under IR demonstrated increased relevant OxPCs particularly fragmented species. OxPC treatment resulted in loss of cardiomyocyte viability, increased mitochondrial permeability when compared to control. EO6 antibody blocked the loss of cardiomyocyte viability. We have shown for the first time that OxPCs are generated cardiomyocytes during IR and they have detrimental effects on cardiomyocyte viability. Additionally the EO6 antibody inhibits the bioactivity of the OxPCs on cardiomyocytes and could be part of a future treatment regimen.en_US
dc.description.noteMay 2015en_US
dc.identifier.citationHasanally, D., R. Chaudhary, A. Ravandi. (2014). Role of Phospholipases and Oxidized Phospholipids in Inflammation. Phospholipases in Health and Disease. P. S. Tappia and N. S. Dhalla, Springer New York. 10: 55-72.en_US
dc.identifier.urihttp://hdl.handle.net/1993/30363
dc.language.isoengen_US
dc.publisherSpringer-Verlag New Yorken_US
dc.rightsopen accessen_US
dc.subjectPhospholipidsen_US
dc.subjectOxidationen_US
dc.subjectCardiomyocytesen_US
dc.subjectIschemiaen_US
dc.subjectReperfusionen_US
dc.subjectLipidomicsen_US
dc.subjectSpectrometryen_US
dc.subjectPhysiologyen_US
dc.subjectCardiologyen_US
dc.subjectMyocardiumen_US
dc.titleBioactive oxidized phosphatidylcholines cause apoptotic cell death in cardiomyocytes during ischemia reperfusionen_US
dc.typemaster thesisen_US
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