Paolo Bernardi
Paolo Bernardi
e-mail:
affiliation: Università di Padova
research area(s): Cell Biology, Chemical Biology
Course: Biosciences and Biotechnologies
University/Istitution: Università di Padova
STUDIES

High School Diploma, Liceo Classico “Paolo Diacono”, Cividale (Italy) 1971
M.D. Degree, University of Padova (Italy), cum laude 1978

APPOINTMENTS

1979 -1987 Assistant Professor, University of Padova, Medical Faculty
1988 -1999 Associate Professor, University of Padova, Medical Faculty
2000 - present Full Professor, University of Padova, Medical Faculty
2001 - 2004 Deputy Dean of the Medical Faculty, University of Padova
2003 - 2009 Director, Department of Biomedical Sciences, University of Padova

HONORS

1984: EMBO Fellow, University of Helsinki, Finland
1985-87: Fogarty Fellow, Whitehead Institute for Biomedical Research, Cambridge MA
2006-2010: Council Member, Bioenergetics Subgroup, Biophysical Society USA
2006-present: Socio Corrispondente, Istituto Veneto di Scienze, Lettere ed Arti
2008: Visiting Professor, Oregon Clin and Transl Res Institute, Portland, OR
2009-2011: Council Member, ABCD
2010-present: President, Italian Group of Biomembranes and Bioenergetics
2010-present: Member, Academia Europaea, Section for Biochemistry and Molecular Biology
2012: Premio Ministro Beni e Attività Culturali per la Fisiologia e Patologia, Accademia Nazionale dei Lincei

FUNDING

Ministry for the University and Scientific Research – Italy; University of Padova; Telethon – Italy; National Institutes of Health - Public Health Service (USA); AIRC (Italian Association on Cancer Research); Association Française contre les Myopathies; Fondazione Cassa di Risparmio di Padova e Rovigo.

BIBLIOMETRIC INDICATIONS

As of May, 2013 Prof. Bernardi has published 189 peer-reviewed articles which have received 17,678 citations with an h index (n of publications with at least n citations) of 67. His most quoted paper [Bernardi P (1999) Mitochondrial transport of cations: Channels, exchangers and permeability transition. Physiol Rev 79, 1127-1155] has 1,121 citations; his most quoted experimental paper [Costantini, P., Chernyak, B.V., Petronilli, V. and Bernardi, P. (1996) Modulation of the Mitochondrial Permeability Transition Pore by Pyridine Nucleotides and Dithiol Oxidation at Two Separate Sites. J. Biol. Chem. 271, 6746-6751] ranks 4th with 471 quotes. His “top ten” list gathers 5,400 quotes.
Paolo Bernardi began his studies on mitochondrial physiology and ion transport under the guidance of Giovanni Felice Azzone, one of the founding Fathers of Bioenergetics. His education in Cellular and Molecular Biology was completed with a long-term stay at the Whitehead Institute for Biomedical Research - Massachusetts Institute of Technology, where he worked under the supervision of Harvey F. Lodish. He pioneered the field of mitochondrial channels and their role in cellular pathophysiology. In particular, he focused on the permeability transition pore (PTP), a high conductance channel that is increasingly recognized as a key player in cell death. During the early 1990s he defined key points of regulation of the PTP in isolated mitochondria (membrane potential, matrix pH, Me2+-binding sites, specific redox-sensitive sites). He then developed tools to reliably monitor mitochondrial function in situ, and addressed mechanistic questions on the PTP as a target in degenerative diseases and cancer cells. His studies have been extended to in vivo models, and culminated with the demonstration that early mitochondrial adaptation plays a key role in hepatocarcinogenesis by 2-acetylaminofluorene [Klöhn et al. (2013) Proc Natl Acad Sci USA 100, 10014-10019] and that muscular dystrophy caused by collagen VI deficiency has an unexpected mitochondrial pathogenesis due to increased PTP opening that can be counteracted by cyclosporin A [Irwin et al (2003) Nat Genet 35, 367-371; Angelin et al. (2007) Proc Natl Acad Sci USA 104, 991-996; Merlini et al. (2008) Proc Natl Acad Sci USA 105, 5225-5229]. Recent key discoveries have been the molecular definition of the PTP, which forms from dimers of the FOF1 ATP synthase in the presence of Ca2+ in a process controlled by cyclophilin D binding to the OSCP subunit [Giorgio et al. (2013) Proc Natl Acad Sci USA 110, 5887-5892]; and that TRAP1 inhibits respiration of cancer cells by decreasing the activity of succinate dehydrogenase, a finding that provides a molecular explanation to the Warburg effect and holds great promise for the selective killing of cancer cells [Sciacovelli et al., Cell Metab (2013) in press].

Paolo Bernardi was a major actor in the Mitochondrial Renaissance of the 1990s. As early as 1992 he was one of the few to realise the importance of mitochondria in cell death well before the role of cytochrome c release was shown to be a key event in apoptosis. He pioneered the field rapidly reaching international recognition, as testified by 159 invited lectures at meetings and 116 seminars at prestigious Institutions worldwide. He has organized or coorganized key meetings on mitochondrial pathophysiology that significantly contributed to the continuing success of the field (2 meetings on New Perspectives in Mitochondrial Research, Padova, Italy 1993 and 1997; Colloquium Mitochondria in Cell Death, 8th European Bioenergetics Conference, Valencia, Spain 1994; Colloquium The Mitochondrial Permeability Transition in Accidental and Programmed Cell Death, 9th European Bioenergetics Conference, Louvain-la-Neuve, Belgium 1996; 1st (1996), 2nd (1998) and 3rd (2000) Conference Frontiers in Mitochondrial Research, Albany, NY; Symposium New Frontiers in Mitochondrial Research – from Bioenergetics to Dynamics, Bertinoro, Italy 2007; 52nd and 54th Annual Meeting of the Biophysical Society USA, Bioenergetics Subgroup Meetings Mitochondria Bioenergetics in Disease and Therapeutics, Long Beach 2008 and Mitochondria in Disease, San Francisco 2010). His achievements were possible through the work and training of junior personnel (from 1991 Prof. Bernardi has supervised the work of 20 Graduate Students from the University of Padova, 4 visiting Graduate Students from other Universities and 11 postdoctoral Fellows).
• Palma, E., Tiepolo, T., Angelin, A., Sabatelli, P., Maraldi, N.M., Basso, E., Forte, M.A., Bernardi, P.* and Bonaldo, P.* (2009) Genetic ablation of cyclophilin D rescues mitochondrial defects and prevents muscle apoptosis in collagen VI myopathic mice, *Corresp auth Hum. Mol. Genet. 18, 2024-2031
• Giorgio, V., Bisetto, E., Soriano, M.E., Dabbeni-Sala, F., Basso, E., Petronilli, V., Forte, M.A., Bernardi, P.* and Lippe, G.* (2009) Cyclophilin D modulates mitochondrial FoF1 ATP synthase by interacting with the lateral stalk of the complex, *Corresp auth, J. Biol. Chem. 284, 33982-33988
• Rasola, A., Sciacovelli, M., Chiara, F., Pantic, B., Brusilow, W.S. and Bernardi, P. (2010) Activation of mitochondrial ERK protects cancer cells from death through inhibition of the permeability transition, Proc. Natl. Acad. Sci. U.S.A. 107, 726-731
• Giorgio, V., Soriano, M.E., Basso, E., Bisetto, E., Lippe, G., Forte, M.A., and Bernardi, P. (2010) Cyclophilin D in Mitochondrial Pathophysiology, Biochim. Biophys. Acta 1797, 1113-1118
• Rasola, A., Sciacovelli, M., Pantic, B. and Bernardi, P. (2010) Signal transduction to the permeability transition pore, FEBS Lett. 584, 1989-1996
• Azzolin, L., von Stockum, S., Basso, E., Forte, M.A. and Bernardi, P. (2010) The mitochondrial permeability transition from yeast to mammals FEBS Lett. 584, 2504-2509
• Azzolin, L., Basso, E., Argenton, F. and Bernardi, P. (2010) Mitochondrial Ca2+ transport and permeability transition in zebrafish (Danio rerio), Biochim. Biophys. Acta 1797, 1775-1779
• Šileikytė, J., Petronilli, V., Zulian, A., Dabbeni-Sala, F., Tognon, G., Nikolov, P., Bernardi, P.* and Ricchelli, F.* (2011) Regulation of the Inner Membrane Mitochondrial Permeability Transition by the Outer Membrane Translocator Protein (Peripheral Benzodiazepine Receptor), *Corresponding Authors, J. Biol. Chem. 286, 1046-1053
• Azzolin, L., Antolini, N., Calderan, A., Ruzza, P., Marin, O., Mammi, S., Bernardi, P., Rasola, A. (2011) Antamanide, a derivative of Amanita phalloides, is a novel desensitizer of the mitochondrial permeability transition pore, PloS One 6, e16280
• Di Lisa, F., Carpi, A., Giorgio, V. and Bernardi, P. (2011) The mitochondrial permeability transition pore and cyclophilin D in cardioprotection, Biochim. Biophys. Acta 1813, 1316-1322
• Ricchelli, F., Šileikytė, J. and Bernardi, P. (2011) Shedding light on the mitochondrial permeability transition, Biochim. Biophys. Acta 1807, 482-490
• Rasola, A. and Bernardi, P. (2011) Mitochondrial permeability transition in Ca2+-dependent apoptosis and necrosis, Cell Calcium 50, 222-233
• Zulian, A., Šileikytė, J., Petronilli, V., Bova, S., Dabbeni-Sala, F., Cargnelli, G., Rennison, D., Brimble, M.A., Hopkins, B., Bernardi, P.*, and Ricchelli., F.* (2011) *Corr Auth, The translocator protein (peripheral benzodiazepine receptor) mediates rat-selective activation of the mitochondrial permeability transition by norbormide, Biochim. Biophys. Acta 1807, 1600-1605
• von Stockum, S., Basso, E., Petronilli, V., Sabatelli, P., Forte, M.A., and Bernardi, P. (2011) Properties of Ca2+ Transport in Mitochondria of Drosophila melanogaster, J. Biol. Chem. 286, 41163-41170
• Giorgio, V., Petronilli, V., Ghelli, A., Carelli, V., Rugolo, M., Lenaz, G., and Bernardi, P. (2012) The Effects of Idebenone on Mitochondrial Bioenergetics, Biochim. Biophys. Acta 1817, 363-369
• Masgras, I., Rasola, A. and Bernardi, P. (2012) Induction of the permeability transition pore in cells depleted of mitochondrial DNA, Biochim. Biophys. Acta 1817, 1860-1866
• Bernardi, P., and von Stockum, S. (2012) The permeability transition pore as a Ca2+ release channel: New answers to an old question, Cell Calcium 52, 22-27
• Nowikovsky, K., Pozzan, T., Rizzuto, R., Scorrano, L. and Bernardi, P. (2012) The Pathophysiology of LETM1, J. Gen. Physiol. 139, 445-454
• Chiara, F., Gambalunga , A., Sciacovelli, M., Nicolli, A., Ronconi, L., Fregona, D., Bernardi, P., Rasola, A., and Trevisan, A. (2012) Chemotherapeutic induction of mitochondrial oxidative stress activates GSK-3α/β and Bax, leading to permeability transition pore opening and tumor cell death, Cell Death Dis. 3, e444
• Giorgio, V., von Stockum, S., Antoniel, M., Fabbro, A., Fogolari, F., Forte, M., Glick, G.D., Petronilli, V., Zoratti, M., Szabó, I., Lippe, G., and Bernardi, P. (2013) Dimers of Mitochondrial ATP Synthase Form the Permeability Transition Pore, Proc. Natl. Acad. Sci. USA 110, 5887-5892
• Sciacovelli, M., Guzzo, G., Morello, V., Frezza, C., Nannini, N., Calabrese, F., Laudiero, G., Esposito, F., Landriscina, M., Gottlieb, E., Defilippi, P., Bernardi, P.* and Rasola, A.* (2013) The mitochondrial chaperone TRAP1 promotes neoplastic growth by inhibiting succinate dehydrogenase, *Corresponding Authors Cell Metab., in press
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