Yves Gouriou

Yves Gouriou is a postdoctoral researcher at Inserm U160-CarMeN laboratory in Lyon, France. His main research focus consists in the identification of new protective strategies in ischemia-reperfusion syndromes (including myocardial infarction, stroke and cardiac arrest) by targeting mitochondria. Yves obtained his PhD in Neuroscience in 2013 at the University of Geneva/Lausanne in the Laboratory of Professor Nicolas Demaurex. During his PhD, he investigated the role of T-type calcium channels in the mitochondrial calcium overload occurring during ischemia (Gouriou et al. Journal of Biological Chemistry, 2013). Following his PhD, he joined the team of Professor Michel Ovize in Lyon and he is investigating the role of ER-mitochondria membrane contact sites in determining mitochondrial fate during ischemia-reperfusion. He is also developing new biosensors to study the deregulation of ion homeostasis in several cellular compartments during cardiac and cerebral ischemia-reperfusion.

Maya Dia

Maya Dia is a PhD student at Inserm U1060-CarMeN laboratory in Lyon, under the direction of Dr Melanie Paillard in the team of Pr Michel Ovize. Her main PhD project focuses on studying the role of reticulum-mitochondria interactions in cardiac ischemia-reperfusion and cardioprotection. The first part of her project consists of studying the alteration of these interactions in metabolic syndrome models (diabetic model), while the second part aims to identify new mitochondrial protective strategies against ischemia-reperfusion injury. Being involved in the Leducq project, Maya is examining the role and regulation of the mitochondrial Ca2+ uniporter during cardiac ischemia-reperfusion as a key player for mitochondrial functioning.

Michael Bround

Michael Bround is a Postdoctoral Research Fellow at Cincinnati Children’s Hospital Medical Center in Cincinnati, USA. Michael’s research is focused on the role of calcium signaling in mitochondrial biology, cell death, and energy metabolism, as well as mitochondrial calcium transport mechanisms. Michael received his PhD in Cellular and Developmental Biology from the University of British Columbia in 2016. His PhD work studied that role of the cardiac calcium channel Ryanodine Receptor 2 (RYR2) and its roles in heart function and cell metabolism. He found that RYR2 plays a significant role in regulating heart rate (Bround et al. Cardiovascular Research 2012) and an important role in stimulating mitochondrial oxidative energy metabolism (Bround et al. The Journal of Biological Chemistry 2013). He further found that RYR2 calcium signaling directly regulates cardiac glucose oxidation rates (Bround et al. The Journal of Biological Chemistry 2016). This work was supported by a UBC doctoral fellowship as well as a CIHR Banting and Best Doctoral Research Award. Following his PhD, Michael Bround joined the research group of Dr. Jeffery Molkentin, an accomplished thought leader in cardiovascular cell biology. There he has contributed to work revealing that importance of the adenine nucleotide transporter family of proteins (ANTs) to the mitochondrial permeability transition pore (MPTP) (Karch*, Bround*, et al. In Revision, Science Advances). This work reveals that MPTP activation requires either the presence of ANT proteins or Cyclophlin D, a known regulator of MPTP, and suggests a model in which the MPTP activity may be comprised of multiple pore forming proteins. He currently works on a variety of projects focusing on mitochondrial calcium signaling and its effects of cell metabolism and necrotic cell death. This work is supported by an American Heart Association Postdoctoral Fellowship.

Moises di Sante

Moises is a senior research associate at the Department of Biomedical Sciences, University of Padova, Italy. His research is primarily focused on the role of mitochondrial biology in cardiomyocyte death, specifically in the identification of the mechanisms of cardiac injury and protection associated to mitochondrial ROS formation. Long-term, Moises would like to comprehensively chart the metabolic changes that occur during heart development and disease. Moises graduated in Biophysics in 2004 and obtained his Ph.D. in Clinical Pharmacology in 2008 from University of Perugia. His Ph.D. work focused on the role of glucocorticoids in stem cells fate decision, showing that spermatogenesis is tightly regulated by corticosteroids and its failure is associated with increased proliferation and aberrant differentiation of undifferentiated spermatogonia (J Biol Chem. 2012 Jan 6;287(2):1242-51.) As a post-doctoral fellow at the Regenerative Medical Center at Brigham and Women’s Hospital (Boston, USA), he collaborated with the team of Professor Mark. A. Perrella to show that mice lacking the Speg gene, a member of the myosin light chain kinase family, develop a cardiomyopathy as a consequence of embryonic defects in cardiac progenitor cell function, that can be rescued by in utero injections of wild-type progenitors into Speg(-/-) foetal hearts (Nature Communications,8825 doi:10.1038/ncomms9825). In 2016 Moises joined the laboratory of Professor Fabio Di Lisa. During this period, he investigated the role Monoamine Oxidases (MAO) during cardiac specification and the regulation of mitochondrial ROS in human cardiomyocytes generated from human induced pluripotent stem cells (hiPSCs). As part of the Leducq project, he is exploring the effect of point mutations on subunits of the FoF1-ATP Synthase in order to gain a better understanding on the role of PTP in cardiomyocyte death.

Tyler Bauer

Tyler Bauer is a medical student working in the Lab of Cardiac Physiology at the National Institutes of Health under the direction of Elizabeth Murphy, PhD. He has completed three years of medical school at Sidney Kimmel Medical College at Thomas Jefferson University Hospital and has been offered a year of research through the Medical Research Scholars Program. During his time in the lab, Tyler developed a model for transmural spectroscopy in the murine ex-vivo perfused heart. He has been applying this modality to ischemia reperfusion injury. As part of the Leducq project, Tyler tested the novel PTP inhibitors produced by the network in the isolated murine heart. Tyler expects to enter the residency match in 2019 in pursuit of a Cardiac Surgery residency

Salvatore Antonucci

Salvatore Antonucci is a Post-Doctoral Researcher at the Department of Biomedical Sciences, University of Padova, Italy. Salvatore’s main research interests include the study of the mechanisms of cardiac injury and protection related to mitochondrial ROS formation and Ca2+homeostasis. He obtained his PhD in Experimental Biomedical Sciences at the University of Padova in 2018. His PhD work focused on the effect of a selective primary increase in mitochondrial ROS levels in cardiomyocytes and supported a hormetic model in which low levels of ROS are cardioprotective while high levels of ROS are cardiotoxic (Antonucci et al, Free Radic Biol Med 2019). During his PhD training, Salvatore was involved in different research fields and publications related to mitochondria (i.e. monoamine oxidases, permeability transition pore, oxidative stress) and their role in cardiac ischaemia/reperfusion injury and diabetic cardiomyopathy. Salvatore continued his post-doctoral training in Prof. Di Lisa’s lab and, among other things, he is investigating the nature of the permeability transition pore and its interplay with mitochondrial ROS that lead to mitochondrial dysfunction. As part of the Leducq project, he is analysing the effect elicited by novel PTP inhibitors developed by the network in cardiomyocytes and he is investigating the point mutations of subunits of the FoF1-ATP Synthase, one of the candidate to form the pore. 

Melanie Paillard

Mélanie Paillard is a postdoctoral researcher at Inserm U160-CarMeN laboratory in Lyon, France. Her main research focus consists in the identification of new protective strategies in ischemia-reperfusion syndromes (including myocardial infarction, stroke and cardiac arrest) by targeting mitochondria. Mélanie graduated from the Ecole Normale Supérieure of Lyon in 2008 and obtained her PhD in Physiology in 2012 from the University Claude Bernard Lyon1. Her PhD work focused on the role of some mitochondrial functions in the mechanisms of cardiomyocyte death during ischemia-reperfusion, notably the reticulum-mitochondria interactions (Paillard el al, Circulation 2013). Mélanie joined the MitoCare center of Pr Gyorgy Hajnoczky in 2013 (Philadelphia, USA), supported by postdoctoral fellowships from Fondation pour la Recherche Médicale and the American Heart Association. During her post-doctoral training, her research led to the discovery of the physio-pathological role of MICU1, a key regulator of the mitochondrial uniporter (Antony*, Paillard* et al., Nat Comm 2016; Paillard et al, Cell Reports 2017), for which she received the Young Bioenergeticist Award in 2017. In order to develop her own translational research program on the regulation of the reticulum-mitochondria interactions during ischemia-reperfusion, Mélanie decided to join the team of Pr Michel Ovize, a recognized expert in the field of cardiovascular clinical research. She is now pursuing her career goal to establish herself as an independent researcher and to manage her translational research program for the development of new protective strategies against ischemia-reperfusion syndromes. Currently, she is investigating the role and regulation of the mitochondrial Ca2+ uniporter during cardiac and cerebral ischemia-reperfusion with her PhD student, Maya Dia.

Justina Šileikytė

Justina is a senior research associate at Vollum Institute, Oregon Health and Science University, Portland, OR. Justina’s main research interests lie in the study of the mitochondrial permeability transition pore (PTP), an inner mitochondrial membrane channel playing a key role in cell death pathways, and thus involved in numerous pathologies, including myocardial infarction and heart failure. Justina obtained her MSc. degree in Biophysics at Vilnius University, Lithuania in 2009. While a student, she wasawarded an Erasmus Fellowship to spent time at University of Padova, Italy, where she began her studies on PTP with Dr. Ricchelli and Dr. P. Bernardi. She continued investigating the regulation and molecular nature of the PTP focusing on contribution of outer mitochondrial membrane to this phenomenon during her graduate studies, and obtained a Ph.D. degree in Cellular Biology in 2013 from University of Padova. Her research focused on the outer mitochondrial membrane and the role of a specific outer membrane protein, TSPO, which at the time was considered an essential component of the PTP. Following genetic inactivation of the gene encoding TSPO, she was able to demonstrate that TSPO, and the entire outer membrane, played no role in the PTP or in mitochondrial bioenergetics (Šileikytė et al., J Biol Chem. 2011 and 2014). 

As a post-doctoral fellow between 2013 and 2016 in P. Bernardi’s laboratory, Justina became interested in high throughput screening of small molecule libraries and took part in an NIH-funded program of Drs. Forte and Bernardi aimed at discovery of novel inhibitors of the PTP. She travelled to Sanford Burnham Medical Research Institute (La Jolla, CA) to screen the NIH MLPCN small molecule library (about 360,000 compounds) and identified a series of novel small molecule inhibitors of the PTP. Subsequently, in collaboration with Dr. F. Schoenen (Kansas University Chemistry Center), secondary chemistry was used to optimise the lead compounds so that the most potent inhibitors of the PTP known to date were generated (Roy,Šileikytė et al., ChemMedChem2015 and 2016; Patent pending). Recently, she has joined Mike Forte's lab in order to refine these molecules to be of use therapeutically as well as identify their binding site(s). 

Georgios Amanakis

Georgios Amanakis is a postdoctoral fellow at the Laboratory of Cardiac Physiology at the National Institutes of Health in Bethesda, USA. His research interest is focused on identifying the underlying cardioprotective mechanisms in myocardial ischemia/reperfusion injury. Georgios received his MD from the Medical School of the University of Crete, Greece in 2008, and then moved to Essen, Germany where he started his residency in internal medicine/cardiology in 2010. During the rotation in the Critical Care and Chest Pain Unit he developed a major interest in limiting myocardial ischemia/reperfusion injury and joined the Institute of Pathophysiology at the University of Duisburg-Essen, Germany, under the direction of Prof. Gerd Heusch to complete his doctoral thesis. His research led to the discovery that cardioprotective ischemic conditioning impacts acutely on the ST-segment elevation in ECG, suggesting protection from ischemic rather than reperfusion injury (Kleinbongard, Amanakis et al, Circ Res 2018; Amanakis et al, Basic Res Cardiol 2019). In 2016, he joined the Laboratory of Cardiac Physiology at the National Institutes of Health, USA, under the direction of Dr. Elizabeth Murphy, a recognized expert in the field of ischemia/reperfusion and mitochondrial permeability transition. He is currently working on identifying redox-sensitive post-translational modifications of cyclophilin-D, a well-known regulator of ischemia/reperfusion injury. His long-term goal is to establish an independent research program focused on translating regulatory mechanisms of myocardial cell-death to the clinic. 

Andrea Urbani

Andrea Urbani is a postdoctoral fellow at the Department of Biomedical Sciences, University of Padova, Italy. Andrea obtained his PhD in Biosciences and Biotechnology, Neurobiology curriculum, at the University of Padova in 2012. During his PhD he investigated, by means of electrophysiology and imaging, the role of astrocyte-neuron crosstalk in migraine in mouse brain slices. Andrea continued his postdoctoral training at the Venetian Institute of Molecular Medicine, Padova, and the Department of Biomedical Sciences. In 2016 Andrea joined Prof. Bernardi’s group, where is currently involved in the electrophysiological characterization of mitochondrial channels by means of planar lipid bilayer reconstitution.

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