{"id":{"repo_id":"vcu","oai_identifier":"oai:scholarscompass.vcu.edu:etd-1105"},"canonical_url":"https://search.dev.ndltd.org/etd/vcu/oai:scholarscompass.vcu.edu:etd-1105","repository":{"repo_id":"vcu","name":"Virginia Commonwealth University","base_url":"https://scholarscompass.vcu.edu/do/oai/"},"display":{"title":"PATHOGENIC ROLE OF PHOSPHODIESTERASE TYPE 5 UPREGULATION IN CARDIAC ISCHEMIA/REPERFUSION INJURY","abstract":"Phosphodiesterase Type 5 (PDE5) inhibitors are cardioprotective against ischemia/reperfusion (I/R) injury. However, it remains uncertain if I/R affects PDE5. We hypothesized that generation of reactive oxygen species (ROS) during I/R leads to upregulation of PDE5, which contributes to pathological changes following acute myocardial infarction (AMI). Adult male ICR mice were subjected to 30 minutes of in vivo or ex vivo I/R. To examine the role of ROS, a subset of hearts were perfused with 100 µM hydrogen peroxide (H2O2). Expression and activity of PDE5, pPDE5, and cGMP-dependent protein kinase (PKG) were measured by Western blots and spectrophotometric assay. The results show that ischemia and I/R significantly increased expression of PDE5. H2O2 had no effect on PDE5 expression and activity but significantly increased PKG activity. We conclude that acute cardiac ischemia or I/R upregulate PDE5 independent of oxidant stress in the heart.","abstract_html":"Phosphodiesterase Type 5 (PDE5) inhibitors are cardioprotective against ischemia/reperfusion (I/R) injury. However, it remains uncertain if I/R affects PDE5. We hypothesized that generation of reactive oxygen species (ROS) during I/R leads to upregulation of PDE5, which contributes to pathological changes following acute myocardial infarction (AMI). Adult male ICR mice were subjected to 30 minutes of in vivo or ex vivo I/R. To examine the role of ROS, a subset of hearts were perfused with 100 µM hydrogen peroxide (H2O2). Expression and activity of PDE5, pPDE5, and cGMP-dependent protein kinase (PKG) were measured by Western blots and spectrophotometric assay. The results show that ischemia and I/R significantly increased expression of PDE5. H2O2 had no effect on PDE5 expression and activity but significantly increased PKG activity. We conclude that acute cardiac ischemia or I/R upregulate PDE5 independent of oxidant stress in the heart.","abstract_has_math":false,"creators":["Hobbs, Daniel"],"institution":null,"degree_name":"Master of Science","degree_level":"Thesis","degree_discipline":"Biochemistry","degree_department":null,"school":null,"contributors":["Rakesh Kukreja"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2010,"date_issued":"2010-07-13T07:00:00Z","date_published":"2010-07-13T07:00:00Z","updated_at":"2026-07-24T05:53:18Z","subjects":["Phosphodiesterase 5","Ischemia/Reperfusion Injury","Reactive Oxygen Species","Pharmacological Preconditioning","cGMP-Dependent Protein Kinase","Myocardial Infarction","Biochemistry, Biophysics, and Structural Biology","Life Sciences"],"languages":[],"rights":["© The Author"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["https://scholarscompass.vcu.edu/etd/106"],"render_values":[{"text":"https://scholarscompass.vcu.edu/etd/106","href":"https://scholarscompass.vcu.edu/etd/106","code":true}]}]},"links":{"outbound_url":"https://doi.org/10.25772/NS9B-2905","outbound_label":"DOI","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Rakesh Kukreja"]},{"key":"dc:creator","label":"Author","values":["Hobbs, Daniel"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2015-07-14T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biochemistry"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Phosphodiesterase 5","Ischemia/Reperfusion Injury","Reactive Oxygen Species","Pharmacological Preconditioning","cGMP-Dependent Protein Kinase","Myocardial Infarction","Biochemistry, Biophysics, and Structural Biology","Life Sciences"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:rights","label":"Dc Rights","values":["© The Author"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://doi.org/10.25772/NS9B-2905","https://scholarscompass.vcu.edu/etd/106"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Phosphodiesterase Type 5 (PDE5) inhibitors are cardioprotective against ischemia/reperfusion (I/R) injury. However, it remains uncertain if I/R affects PDE5. We hypothesized that generation of reactive oxygen species (ROS) during I/R leads to upregulation of PDE5, which contributes to pathological changes following acute myocardial infarction (AMI). Adult male ICR mice were subjected to 30 minutes of in vivo or ex vivo I/R. To examine the role of ROS, a subset of hearts were perfused with 100 µM hydrogen peroxide (H2O2). Expression and activity of PDE5, pPDE5, and cGMP-dependent protein kinase (PKG) were measured by Western blots and spectrophotometric assay. The results show that ischemia and I/R significantly increased expression of PDE5. H2O2 had no effect on PDE5 expression and activity but significantly increased PKG activity. We conclude that acute cardiac ischemia or I/R upregulate PDE5 independent of oxidant stress in the heart."]},{"key":"dc:title","label":"Title","values":["PATHOGENIC ROLE OF PHOSPHODIESTERASE TYPE 5 UPREGULATION IN CARDIAC ISCHEMIA/REPERFUSION INJURY"]}]}],"canonical_facts":{"dc:contributor":["Rakesh Kukreja"],"dc:creator":["Hobbs, Daniel"],"dc:date.available":["2015-07-14T07:00:00Z"],"dc:description.abstract":["Phosphodiesterase Type 5 (PDE5) inhibitors are cardioprotective against ischemia/reperfusion (I/R) injury. However, it remains uncertain if I/R affects PDE5. We hypothesized that generation of reactive oxygen species (ROS) during I/R leads to upregulation of PDE5, which contributes to pathological changes following acute myocardial infarction (AMI). Adult male ICR mice were subjected to 30 minutes of in vivo or ex vivo I/R. To examine the role of ROS, a subset of hearts were perfused with 100 µM hydrogen peroxide (H2O2). Expression and activity of PDE5, pPDE5, and cGMP-dependent protein kinase (PKG) were measured by Western blots and spectrophotometric assay. The results show that ischemia and I/R significantly increased expression of PDE5. H2O2 had no effect on PDE5 expression and activity but significantly increased PKG activity. We conclude that acute cardiac ischemia or I/R upregulate PDE5 independent of oxidant stress in the heart."],"dc:identifier":["https://doi.org/10.25772/NS9B-2905","https://scholarscompass.vcu.edu/etd/106"],"dc:rights":["© The Author"],"dc:subject":["Phosphodiesterase 5","Ischemia/Reperfusion Injury","Reactive Oxygen Species","Pharmacological Preconditioning","cGMP-Dependent Protein Kinase","Myocardial Infarction","Biochemistry, Biophysics, and Structural Biology","Life Sciences"],"dc:title":["PATHOGENIC ROLE OF PHOSPHODIESTERASE TYPE 5 UPREGULATION IN CARDIAC ISCHEMIA/REPERFUSION INJURY"],"thesis:degree_discipline":["Biochemistry"],"thesis:degree_level":["Thesis"],"thesis:degree_name":["Master of Science"]},"updated_at":"2026-07-24T05:53:18Z"}