Rigoni MichelaAssociate Professor of Pathology Dept. of Biomedical SciencesUniversity of Paduamichela.rigoni@unipd.itStudiesHigh School Diploma. Secondary studies specialized on humanities and modern languagesMaster Degree in Biological Sciences, UnipdPhD in Cellular and Molecular Biology and Pathology, UnipdTeaching activities:Present Lectures (Unipd)Pathophysiology and General Pathology for the Bachelor Degree in Human Movement Sciences, School of MedicineGeneral Pathology for the Bachelor Degree in Biotechnology, School of ScienceHistopathology for the Master Degree in Medicine and Surgery, School of Medicine Past Lectures (Unipd)General Pathology for the Master Degree in Medicine and Surgery, School of MedicineGeneral Pathology for the Master Degree in Dentistry and Dental Prosthetics, School of MedicineGeneral Pathology for the Bachelor Degree in Medical Functional Diagnostics Technician, School of MedicineGeneral Pathology for the Bachelor Degree in Nursery, School of MedicineMolecular Pathology for the Master Degree in Medical Biology, School of ScienceHistopathology for the Master Degree in Medical Biology, School of ScienceSupervisor of bachelor, master, PhD students and postdoctoral fellowsCurrent research interests: NeuroregenerationContributions to Science1)During my Master thesis in Biological Sciences, I worked on Clostridial neurotoxins, and clarified the role of specific residues of their light chains in their enzymatic activity.2)During my PhD and my post-doctoral training, I dissected the mechanism of action of a class of presynaptic neurotoxins from Elapid snakes endowed with PLA2 activity. I discovered that, by cleaving phospholipids of the presynaptic plasma membrane, they generate lysophospholipids and fatty acids that alter the energetics of the membrane, thus affecting its disposition to bend and fuse with synaptic vesicles. These results deserved a Perspective in Science by Zimmemberg and Chernomoridik, pioneers in the study of membrane fusion. Moreover, by altering plasma membrane permeability, they induce a toxic calcium influx within nerve terminals, which in turn triggers nerve terminal degeneration and paralysis of the NMJ. 3)Since 2009, I expanded my interests from basic to more translational neuroscience. I exploited presynaptic neurotoxins to set up an innovative experimental approach to study regeneration of the NMJ. Indeed, the neuroparalysis induced by some of these toxins is rapid and reversible in a few days, making these toxins a powerful tool to study within a short time window the molecular mechanisms underlying peripheral nerve regeneration following an acute degeneration. I identified hydrogen peroxide produced by mitochondria of injured neurons as a major signaling molecule driving Schwann cells’ (SC) activation. Moreover, by combining transcriptomics, electrophysiology and imaging, I am currently investigating the cross-talk taking place at the murine NMJ between damaged nerve terminals, terminal SC and the muscle, to identify molecules and pathways promoting nerve terminal recovery of function to be tested in different peripheral neuropathies, in a therapeutic perspective. I recently I found that the CXCL12α-CXCR4 and melatonin-MT1 signaling axes are crucial for successful peripheral nerve terminal regeneration following acute forms of nerve injuries. I am trying to translate this knowledge to chronic neurodegenerative conditions (e.g. ALS).

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