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People ■ Paola Magotti
Paola Magotti's foto

Paola Magotti

Post Doc

iit / Drug Discovery and Development

Phone +39 010 71781711

Bio

Paola Magotti graduated in Industrial Biotechnology at the University of Modena and Reggio Emilia in 2003. She started her research experience in January 2002 in the laboratory of Dr. Luca Forti where she was involved in a project based on the development of improved analogs of resveratrol, a polyphenol found in red wine that shows promising antioxidant and antiproliferative properties.
For her Ph.D fellowship she joined in 2004 the laboratory of Dr. John D. Lambris at the University of Pennsylvania.
Her Ph.D thesis focused on both molecular and functional aspects of inhibitors of the central molecule of the complement system, C3. Paola worked on several projects that included the development of protein-based complement inhibitors and the functional characterization of a complement evasion protein from staphylococcus aureus.
From 2008 to August 2009 she continued to work in Dr Lambris lab as a post doctoral fellow and she conducted her own research focused on the biophysical characterization of the peptide-based complement inhibitor compstatin and identified its important structural features, to support the development of analogs with improved efficacy.
As a result of her experience, Paola has become an expert in a broad panel of biochemical and biophysical approaches such as Mass spectrometry (MALDI-Tof and ESI), Isothermal titration calorimetry (ITC) and surface plasmon resonance (SPR), for the characterization of molecular interactions.
In September 2009 Paola joined the IIT Drug Discovery unit as a junior post doc.
Paola Magotti graduated in Industrial Biotechnology at the University of Modena and Reggio Emilia in 2003. She started her research experience in January 2002 in the laboratory of Dr. Luca Forti where she was involved in a project based on the development of improved analogs of resveratrol, a polyphenol found in red wine that shows promising antioxidant and antiproliferative properties.
For her Ph.D fellowship she joined in 2004 the laboratory of Dr. John D. Lambris at the University of Pennsylvania.
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Projects

Imbalances of human major lipid signaling pathways contribute to progression in neurodegenerative diseases, metabolic diseases, and inflammation. Among lipidic messengers, the family of bioactive N-Acylethanolamines (NAEs) is agonist at cannabinoid and nuclear α-type peroxisome proliferator-activated receptors. The ability of NAEs and their metabolic enzymes to modulate neurotransmission and a variety of pathophysiological processes, including inflammation, appetite, pain and mood, provides unique chances for drug discovery. When human cell are stimulated, bioactive NAEs are generated from membranes in a two-step pathway, which involves an N-acyltransferase and an N-acylphosphatidylethanolamine-hydrolyzing phospholipase D (NAPE-PLD). NAEs bearing saturated and monounsaturated long acyl chains are significantly decreased in NAPE-PLD(-/-) mice suggesting this enzymes as  key regulators of the NAE-mediated signaling potential. Very little is known about the molecular architecture of NAPE-PLD and the specific functional role of its N- and C-terminal domains. My goal is to study trafficking in activated cells and solve the X-ray structure of this membrane-bound protein. I will characterize the thermodynamics and kinetics of enzyme interactions, which are essential in understanding how NAPE-PLD synthesizes NEAs and controls their cellular level. Findings will be used for a rational approach in the design of potent and selective NAPE-PLD ligands, which can be exploited pharmacologically to modulate the level of NAEs in inflammation, pain, and neurodegenerative disorders. It is a common goal of cell biology, structural biology, pharmacology, and medicinal chemistry, which could give an invaluable blueprint for the design of selective inhibitors.

Imbalances of human major lipid signaling pathways contribute to progression in neurodegenerative diseases, metabolic diseases, and inflammation. Among lipidic messengers, the family of bioactive N-Acylethanolamines (NAEs) is agonist at cannabinoid and nuclear α-type peroxisome proliferator-activated receptors. The ability of NAEs and their metabolic enzymes to modulate neurotransmission and a variety of pathophysiological processes, including inflammation, appetite, pain and mood, provides unique ...

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Selected Publications

1)      Magotti P, Qu H, Ricklin D, Wu Y, Kourtzelis I and Lambris JD
Improving Compstatin Potency Via Peptide Backbone Mono-N-Methylation. Mol Immunol. 2011 Jan;48(4):481-9. Epub 2010 Nov
2)      Wang M, Krauss JL, Domon H, Hosur KB, Liang S, Magotti P, Triantafilou M, Triantafilou K, Lambris JD, Hajishengallis G.
Microbial hijacking of complement-toll-like receptor crosstalk.
Sci signal. 2010 Feb 16;3(109):ra11
3)      Georgopoulos LJ, Elgue G, Sanchez J, Dussupt V, Magotti P, Lambris JD, Tötterman TH, Maitland
Preclinical evaluation of innate immunità to baculovirus gene therapy vectors in whole human blood. Mol Immunol. 2009 Sep;46(15):2911-7. Epub 2009 Aug 8
4)      Magotti P, Ricklin D, Qu H, Wu Y, Kaznessis Y, Lambris JD
Structure-Kinetic Relationship Analysis of the Therapeutic Complement Inhibitor Compstatin.
Journal of molecular recognition
5)      Garrett MC, Otten ML, Starke RM, Komotar RJ, Magotti P, Lambris JD, Rynkowski MA, Connolly ES.
Synergistic neuroprotective effects of C3a and C5a receptor blockade following intracerebral  hemorrhage.
Brain Res. 2009 May 3. [Epub ahead of print]
6)      Hamad OA, Nilsson-Ekdahl K, Nilsson P, Andersson J, Magotti P, Lambris JD, Nilsson B
Complement activation is triggered by chondroitin sulfate released by thrombin receptor- activated   platelets
J Thromb Haemost. 2008 Aug;6(8):1413-21. Epub 2008 May 2
7)      Kambas K, Markiewski MM, Pneumatikos IA, Rafail SS, Theodorou V, Konstantonis D, Kourtzelis I,  Doumas    MN, Magotti P, Deangelis RA, Lambris JD, Ritis KD
C5a and TNF-alpha up-regulate the expression of tissue factor in intra-alveolar neutrophils of    patients with the  acute respiratory distress syndrome
J Immunol. 2008 Jun 1;180(11):7368-75
8)      Saethre M, Schneider MK, Lambris JD, Magotti P, Haraldsen G, Seebach JD, Mollnes TE
Cytokine secretion depends on Galalpha(1,3)Gal expression in a pig-to-human whole blood model
J Immunol. 2008 May 1;180(9):6346-53
9)      Lappegard KT, Bergseth G, Riesenfeld J, Pharo A, Magotti P, Lambris JD, Mollnes TE
The artificial surface-induced whole blood inflammatory reaction revealed by increases of chemokines  and   growth  factors is largely complement dependent
Journal of biomedical materials research: Part A, 2007 Dec. 17
10) Hammel M, Sfyroera G, Ricklin D, Magotti P, Lambris JD, Geisbrecht BV
A structural basis for complement inhibition by Staphylococcus aureus
Nat Immunol. 2007 Apr;8(4):430-7.
11) Ritis K, Doumas M, Mastellos D, Micheli A, Giaglis S, Magotti P, Rafail S, Kartalis G, Sideras P,   Lambris JD
A novel C5a receptor-tissue factor cross-talk in neutrophils links innate immunity to coagulation   pathways
J Immunol. 2006 Oct 1;177(7):4794-802
12)  Katragadda M, Magotti P, Sfyroera G, Lambris J.D
Hydrophobic effect and hydrogen bonds account for the improved activity of a complement inhibitor, compstatin
J Med Chem. 2006 Jul 27;49(15):4616-22

1)      Magotti P, Qu H, Ricklin D, Wu Y, Kourtzelis I and Lambris JD
Improving Compstatin Potency Via Peptide Backbone Mono-N-Methylation. Mol Immunol. 2011 Jan;48(4):481-9. Epub 2010 Nov
2)      Wang M, Krauss JL, Domon H, Hosur KB, Liang S, Magotti P, Triantafilou M, Triantafilou K, Lambris JD, Hajishengallis G.
Microbial hijacking of complement-toll-like receptor crosstalk.
Sci signal. 2010 Feb 16;3(109):ra11
3)      Georgopoulos LJ, Elgue G, Sanchez J, Dussupt V, Magotti P, Lambris JD, ...

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