Rigoni Michela
Associate Professor of Pathology
Dept. of Biomedical Sciences
University of Padua
michela.rigoni@unipd.it
Studies
High School Diploma. Secondary studies specialized on humanities and modern languages
Master Degree in Biological Sciences, Unipd
PhD in Cellular and Molecular Biology and Pathology, Unipd
Teaching activities:
Present Lectures (Unipd)
Pathophysiology and General Pathology for the Bachelor Degree in Human Movement Sciences, School of Medicine
General Pathology for the Bachelor Degree in Biotechnology, School of Science
Histopathology 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 Medicine
General Pathology for the Master Degree in Dentistry and Dental Prosthetics, School of Medicine
General Pathology for the Bachelor Degree in Medical Functional Diagnostics Technician, School of Medicine
General Pathology for the Bachelor Degree in Nursery, School of Medicine
Molecular Pathology for the Master Degree in Medical Biology, School of Science
Histopathology for the Master Degree in Medical Biology, School of Science
Supervisor of bachelor, master, PhD students and postdoctoral fellows

Current research interests: Neuroregeneration

Contributions to Science
1) 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).

Notices