Articolo in rivista, 2021, ENG, 10.1016/j.nbd.2021.105538
Valentina La Cognata; Elisabetta Golini; Rosario Iemmolo; Sara Balletta; Giovanna Morello; Carla De Rosa; Ambra Villari; Sara Marinelli; Valentina Vacca; Gabriele Bonaventura; Paola Dell'Albani; Eleonora Aronica; Fabio Mammano; Silvia Mandillo; Sebastiano Cavallaro;
Institute for Biomedical Research and Innovation, National Research Council, Via P. Gaifami 18, Catania, CT, 95126, Institute for Biomedical Research and Innovation, National Research Council, Via P. Gaifami 18, 95126, Catania (CT), Italy, , Italy; Institute of Biochemistry and Cell Biology, National Research Council, Via E. Ramarini 32, Monterotondo Scalo, RM, 00015, Institute of Biochemistry and Cell Biology, National Research Council, Via E. Ramarini 32, 00015, Monterotondo scalo (RM), Italy, , Italy; Department of (Neuro) Pathology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Meibergdreef 9, Amsterdam, 1105, Department of (Neuro)Pathology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Meibergdreef 9, 1105 Amsterdam, The Netherlands, , , Netherlands; Department of (Neuro) Pathology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Meibergdreef 9, Amsterdam, 1105, Department of (Neuro)Pathology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Meibergdreef 9, 1105 Amsterdam, The Netherlands, , , Netherlands; Department of Physics and Astronomy "G. Galilei", University of Padua, Padova, Department of Physics and Astronomy "G. Galilei", University of Padua, Padova, Italy, , Italy
Amyotrophic Lateral Sclerosis (ALS) is a progressive neurodegenerative disease characterized by depletion of motor neurons (MNs), for which effective medical treatments are still required. Previous transcriptomic analysis revealed the up-regulation of C-X-C motif chemokine receptor 2 (CXCR2)-mRNA in a subset of sporadic ALS patients and SOD1G93A mice. Here, we confirmed the increase of CXCR2 in human ALS cortex, and showed that CXCR2 is mainly localized in cell bodies and axons of cortical neurons. We also investigated the effects of reparixin, an allosteric inhibitor of CXCR2, in degenerating human iPSC-derived MNs and SOD1G93A mice. In vitro, reparixin rescued MNs from apoptotic cell death, preserving neuronal morphology, mitochondrial membrane potential and cytoplasmic membrane integrity, whereas in vivo it improved neuromuscular function of SOD1G93A mice. Altogether, these data suggest a role for CXCR2 in ALS pathology and support its pharmacological inhibition as a candidate therapeutic strategy against ALS at least in a specific subgroup of patients.
Neurobiology of disease 160
CXCR2, Amyotrophic lateral sclerosis, IL8, iPSC, Motor neurons, Neurodegeneration, Reparixin, SOD1G93A mouse
Iemmolo Rosario, Morello Giovanna, Bonaventura Gabriele, Villari Ambra, Vacca Valentina, Cavallaro Sebastiano, Dell Albani Paola, Golini Elisabetta, Mandillo Silvia, Marinelli Sara, Mammano Fabio, La Cognata Valentina
IRIB – Istituto per la Ricerca e l'Innovazione Biomedica, IBBC – Istituto di Biochimica e Biologia Cellulare
ID: 459153
Year: 2021
Type: Articolo in rivista
Creation: 2021-11-19 10:40:03.000
Last update: 2022-08-25 12:45:35.000
External links
OAI-PMH: Dublin Core
OAI-PMH: Mods
OAI-PMH: RDF
DOI: 10.1016/j.nbd.2021.105538
URL: http://www.scopus.com/record/display.url?eid=2-s2.0-85118493557&origin=inward
External IDs
CNR OAI-PMH: oai:it.cnr:prodotti:459153
DOI: 10.1016/j.nbd.2021.105538
Scopus: 2-s2.0-85118493557