Michelangelo Campanella
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Michelangelo is a Lecturer in Pharmacology. Michelangelo's most recent research aims to assess the role if the IF-1 protein in pathologies due to mitochondrial mutations and in tumours.
Biography
Michelangelo began his studies with a degree as Doctor of Pharmacy at the University of Ferrara School of Pharmacy, Italy. The course focused on the knowledge and clinical usage of therapeutics and the comprehension of their pharmacological basis and protocols of preparation.
In the last two years of his degree, Michelangelo joined the lab of Professor Rosario Rizzuto to undertake his undergraduate research project focused on the development and learning of luminescence based approaches to monitor Ca2+ and ATP signals in living cells. Prof. Rizzuto is one of the world experts in Ca2+ signalling who also has the merit of identifying mitochondria as a relevant pathway for the definition of Ca2+ homeostasis.
Michelangelo also worked at the Columbia University of New York in the lab of Professor Eric Schon, a luminary figure engaged in the clarification of the mitochondrial genetic, who taught him the principles and the basal techniques of molecular biology. Upon completion of his degree, Michelangelo registered to the Italian Pharmaceutical Society to practise as a Pharmacist.
Following a short period in practice, he began a PhD in Cellular and Molecular Pharmacology still under the supervision of Prof. Rizzuto. His PhD work was centred on the role of Ca2+ in programmed cell death. After concluding his PhD, Michelangelo was keen to undertake further training so he moved abroad and joined the lab of Professor Michael R Duchen at the University College London. Prof. Duchen is an eminent scientist renowned for his work on mitochondrial physiology and his unique competence of imaging techniques.
During his period at UCL Michelangelo received initial support from the Royal Society, Accademia dei Lincei and the European Molecular Biology Organization (EMBO) before being awarded of a Marie Curie Intra-european Fellowship which allowed him to complete a research period lasting 3 years. During this time he was also honoured of the opportunity to attend the Lindau meeting of Nobel prizes in Physiology as a young promising scientist in the field. Although Michelangelo moved to the Royal Veterinary College in February 2008 as a Lecturer in Pharmacology, he still holds an honorary position at UCL.
Research
Michelangelo’s principal research aim is to characterize the cell biological role of mitochondrial proteins which may represent a valuable therapeutic target in pathological conditions. Mitochondria have been for years the preserve of biochemists and just recently they become of interest for cell biologists due to their role in cell signalling and so in the definition of global cellular physiology and pathology. In light of this Michelangelo would like to take this further and make them a topic of high relevance for pharmacologists and for the design of novel therapeutic agents.
He is currently engaged in studying the physiological and pathological role of the mitochondrial ATP ase inhibitory factor 1, IF1. IF1 principal function is to avoid ATP consumption driven by mitochondria when the respiration is impaired besides –as very recently discovered- being able to regulate basic mitochondrial function and structure. Michelangelo would like therefore to assess now the protein role in programmed cell death and in pathologies due to mitochondrial mutations wherein ATP consumption represents a relevant pathological mechanism. Ultimately, he aims to design a peptide able to regulate IF1 activity which can be eventually employed for clinical purposes.
Alongside his IF1 work, Michelangelo is now starting a new line of research looking at the mitochondrial benzodiazepine receptor (mBzR) cell biological role. He is indeed keen to understand how the expression level of mBzR can affect mitochondrial function and consequently the whole cellular physiology and susceptibility to cell death induction. It is indeed established that mBzR is over-expressed in tumours and so involved in the counteraction of the chemotherapeutic drugs efficiency. However, the mechanism by which it exerts such functions remains ill-defined and particularly how this is reflected on mitochondrial homeostasis.
Michelangelo’s main collaboration is with Prof. M. Duchen at the Department of Physiology, UCL, exploring IF1 further, however he also has ongoing collaborations with clinicians at the Institute of Child Health (Dr. Paolo de Coppi) and at the Institute of Neurology UCL (Prof. Mike G. Hanna) with whom he is studying mitochondria function in stem cells and exploring the ATP consumption as pathogenetic mechanism in diseases of mitochondrial origin respectively.
Teaching
Michelangelo will be teaching antimicrobials on the BVetMed course.
Clinical
Michelangelo hopes to define novel pharmacological targets to obtain improvement of various pathological conditions.
Selected Publications
CAMPANELLA, M., CASSWELL, E., CHONG, S., FARAH, Z., WIECKOWSKI, M. R., ABRAMOV, A. Y., TINKER, A. & DUCHEN, M. R. (2008) Regulation of mitochondrial structure and function by the F1Fo-ATPase inhibitor protein, IF1. Cell Metab 8, 13-25. PubMed ID 18590689
MCKENZIE, M., LIOLITSA, D., AKINSHINA, N., CAMPANELLA, M., SISODIYA, S., HARGREAVES, I., NIRMALANANTHAN, N., SWEENEY, M. G., ABOU-SLEIMAN, P. M., WOOD, N. W., HANNA, M. G. & DUCHEN, M. R. (2007) Mitochondrial ND5 gene variation associated with encephalomyopathy and mitochondrial ATP consumption. J Biol Chem 282, 36845-36852. PubMed ID 17940288
HOYER-HANSEN, M., BASTHOLM, L., SZYNIAROWSKI, P., CAMPANELLA, M., SZABADKAI, G., FARKAS, T., BIANCHI, K., FEHRENBACHER, N., ELLING, F., RIZZUTO, R., MATHIASEN, I. S. & JAATTELA, M. (2007) Control of macroautophagy by calcium, calmodulin-dependent kinase kinase-beta, and Bcl-2. Mol Cell 25, 193-205. PubMed ID 17244528
CHAMI, M., PRANDINI, A., CAMPANELLA, M., PINTON, P., SZABADKAI, G., REED, J. C. & RIZZUTO, R. (2004) Bcl-2 and Bax exert opposing effects on Ca2+ signaling, which do not depend on their putative pore-forming region. J Biol Chem 279, 54581-54589. PubMed ID 15485871
CAMPANELLA, M., PINTON, P. & RIZZUTO, R. (2004) Mitochondrial Ca2+ homeostasis in health and disease. Biol Res 37, 653-660. PubMed ID 15709694
CAMPANELLA, M., DE JONG, A. S., LANKE, K. W., MELCHERS, W. J., WILLEMS, P. H., PINTON, P., RIZZUTO, R. & VAN KUPPEVELD, F. J. (2004) The coxsackievirus 2B protein suppresses apoptotic host cell responses by manipulating intracellular Ca2+ homeostasis. J Biol Chem 279, 18440-18450. PubMed ID 14976205
AGUIARI, G., CAMPANELLA, M., MANZATI, E., PINTON, P., BANZI, M., MORETTI, S., PIVA, R., RIZZUTO, R. & DEL SENNO, L. (2003) Expression of polycystin-1 C-terminal fragment enhances the ATP-induced Ca2+ release in human kidney cells. Biochem Biophys Res Commun 301, 657-664. PubMed ID 12565830
FERRARI, D., PINTON, P., SZABADKAI, G., CHAMI, M., CAMPANELLA, M., POZZAN, T. & RIZZUTO, R. (2002) Endoplasmic reticulum, Bcl-2 and Ca2+ handling in apoptosis. Cell Calcium 32, 413-420. PubMed ID 12543100