Protein Kinase Beta II (PKC-βІI) inhibitor exerts cardioprotective effects in Myocardial Ischemia/Reperfusion Injury (MI/R)
Date of Award
Master of Science in Biomedical Sciences
Lindon Young, PhD
Qian Chen, PhD
Cathy Hatcher, PhD
During myocardial ischemia/reperfusion (I/R), the generation of reactive oxygen species (ROS) contributes to the post-reperfused cardiac injury and contractile dysfunction. Activation of Protein Kinase C beta II (PKC βII) has been associated with increased ROS release from myocardial I/R tissue, decreased endothelial-derived nitric oxide, and increased infarct size. We tested the hypothesis that using a cell permeable PKC βII peptide inhibitor (PKC βII-) (N-myr-SLNPEWNET, MW=1300 g/mol, 10μM or 20μM) will attenuate infarct size and improve post-reperfused cardiac function compared to untreated controls in isolated perfused rat hearts subjected to I(30min)/R(90 min). PKC βII- treated hearts (both 10 and 20 μM) significantly improved postreperfused cardiac function (e.g. left ventricular developed pressure [LVDP], and dP/dt max) compared to controls (all p
Lipscombe, Christina G., "Protein Kinase Beta II (PKC-βІI) inhibitor exerts cardioprotective effects in Myocardial Ischemia/Reperfusion Injury (MI/R)" (2019). PCOM Biomedical Studies Student Scholarship. 175.