Radical species, mitochondria and cardiac function
Sponsored by the SEB Animal Section
Session organizers: Maria Carmela Cerra and Bruno Tota, University of Calabria, Italy
Increasing evidence is emerging that reactive oxygen species (ROS), rather than being only the unwanted by-products of the aerobic biome in which they are responsible for oxidative damage, are also essential components of signal cascades important in sensing environmental changes and orchestrating a variety of tightly regulated responses. At sub-cellular level, mitochondria play a major role in coordinating these responses, including the activation of cell survival programs. Several oxidant-sensitive transcription factors, able to activate gene expression in response to oxidative stressful conditions, are implicated in the cross talk between nucleus and mitochondria.
Due to its very nature the heart, an aerobic continuously contracting organ, is an extremely challenging conceptual model for exploring the complexity and wonder of these homeostatic cascades. It also epitomises how physiology and pathology can be two facets of the same issue. In fact, ROS research is gaining momentum in basic and clinically oriented cardiovascular investigations. Central players are Janus-faced endogenous ROS producing gases, i.e. Nitric Oxide and Hydrogen Sulfide. Although being physiological signalling agents in cardiac cells, their misregulated generation leads to oxidative stress and free radical damage, requiring the activation of protection programmes to prevent mitochondrial dysfunction and myocardial injury or death.
This session will focus on different aspects, which underlie the interplay between ROS, mitochondria and cardiac biology in vertebrates. Examples from different organisms will illustrate the unity and diversity of fundamental homeostatic processes. The goal is to stimulate interdisciplinary discussion and cross talk among scientists working in this expanding area of research.
Session Programme - Wednesday 9th July
09:00 Prof. Fabio Di Lisa (University of Padova)
Mitochondrial ROS formation and myocardial injury [A7.1]
09:30 Dr David Wink (National Cancer Institute)
Biochemistry of NO and RNOS in ischemia and reperfusion injury [A7.2]
10:00 To be confirmed
10:30 Prof. Barbara Casadei (John Radcliffe Hospital)
Constitutive NO production in the myocardium: more than cGMP signalling [A7.4]
11:00 Refreshment Break
11:30 Dr Frank B Jensen (University of Southern Denmark)
Nitric oxide production from nitrite in fish: mechanisms and physiological implications [A7.5]
12:00 Prof. Bruno Tota (University of Calabria)
Nitrite modulation of cardiac contractility in vertebrate hearts [A7.6]
12:30 Lunch
14:00 Dr Georg Kojda (Institute of Pharmacology, University Hospital, Duesseldorf)
Reactive oxygen species as cardiovascular mediators: lessons from transgenic mice [A7.7]
14:30 Dr Pasquale Pagliaro (Università di Torino)
ROS in cardiac ischemic pre- and post-conditioning [A7.8]
15:00 Refreshment Break
15:30 Dr Kenneth R. Olson (Indiana University School of Medicine)
Oxygen sensing or just passing gas: hydrogen sulfide as the mediator of cardiovascular responses to hypoxia [A7.9]
16:00 Dr Daniele Mancardi (Università di Torino)
Involvement of mitochondria in the protective effect of Hydrogen Sulfide against oxidative stress incardiomyocytes [A7.10]
16:30 Dr Richard Handy (University of Plymouth)
The effects of carbon monoxide and hyperbaric oxygen on the cardiovascular system [A7.11]
17:00 Concluding Remarks
Each presentation: 25 min plus 5 min discussion
