Conference registration is mandatory for consideration of the abstract by the Scientific committee for oral and/or poster presentation. Abstracts must be original and must not have been published or presented at any international meeting. By submitting an abstract, the author transfers copyright ownership to the organizing committee for publications; the Organizing Committee reserves the right to reproduce the abstract in print and/or electronic media.
Deadline for submission for consideration for oral presentation: June 15, 2020.
Deadline for submission for consideration for poster presentation: July 1, 2020.
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Sample abstract included below:
Reactive oxygen species (ROS) in cardioprotection: which ROS does the signaling?
Anders O. Garlid¹, Matthew Gold¹, Martin Jaburek², and Keith D. Garlid¹
¹Portland State University, Dept. of Biology Portland OR, USA (firstname.lastname@example.org)
²Dept. of Membrane Transport Biophysics, Institute of Physiology, Prague, Czech Republic
ROS are the second messengers of cardioprotective signaling; however, the ROS species responsible for this effect under physiological conditions is not known. Cellular ROS transformations proceed from superoxide (O₂-) to hydrogen peroxide (H₂O₂) and then to hydroxyl radical (•OH), each of which has been investigated as the signaling ROS. H₂O₂ is an appealing candidate for a second messenger because it is relatively stable and can readily diffuse to target kinases. Nevertheless, there is no direct evidence to support or exclude H₂O₂ as the physiological ROS messenger. We examined the effects of exogenous H₂O₂ and endogenous (mitochondrial) ROS produced by the electron transport chain on three ROS-dependent processes: PKCε-dependent mitochondrial ATP-sensitive potassium channel (mitoKATP) opening, PKCε-dependent inhibition of the mitochondrial permeability transition (MPT), and cardioprotection of the ex vivo heart. Dimethylsulfoxide (DMSO) and dimethylformamide (DMF) scavenge •OH but neither influenced PKCε activation by exogenous H₂O₂. This indicates that they neither scavenge H₂O₂ nor are they thiol reductants. However, both reagents blocked PKCe activation by endogenous (mitochondrial) ROS, and DMF blocked cardioprotection by diazoxide and ischemic postconditioning. The putative •OH scavenger N-2-mercaptopropionylglycine (MPG) blocked PKCε activation by exogenous H₂O₂, indicating that MPG is acting here as a thiol reductant rather than as a ROS scavenger. These results appear to exclude H₂O₂ as the signaling ROS and implicate a downstream oxidation product of •OH. Our evidence points to hydroperoxy fatty acids as the signaling ROS in cardioprotection.
Keywords: mitochondria; cardioprotection; hydroxyl radical; K-ATP channels; cardiac ischemia; hydroperoxy fatty acids; ROS signaling
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