Schwann cell autophagy counteracts the onset and chronification of neuropathic pain (Articolo in rivista)

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  • Schwann cell autophagy counteracts the onset and chronification of neuropathic pain (Articolo in rivista) (literal)
Anno
  • 2014-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1016/j.pain.2013.09.013 (literal)
Alternative label
  • Marinelli S.1; Nazio F.1; Tinari A.3; Ciarlo L.4; D'Amelio M.5; Pieroni L.6; Vacca V.1; Urbani A.6; Cecconi F.7; Malorni W.8; Pavone F.9 (2014)
    Schwann cell autophagy counteracts the onset and chronification of neuropathic pain
    in Pain (Amst. Online)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Marinelli S.1; Nazio F.1; Tinari A.3; Ciarlo L.4; D'Amelio M.5; Pieroni L.6; Vacca V.1; Urbani A.6; Cecconi F.7; Malorni W.8; Pavone F.9 (literal)
Pagina inizio
  • 93 (literal)
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  • 107 (literal)
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Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 155 (literal)
Rivista
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  • 1 (literal)
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  • Scopu (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • 1 CNR - National Research Council, Cell Biology and Neurobiology Institute, Rome, Italy; Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Fondazione Santa Lucia, Rome, Italy. 2 Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Fondazione Santa Lucia, Rome, Italy. 3 Department of Technology and Health, Istituto Superiore di Sanita', Rome, Italy. 4 Department of Therapeutic Research and Medicine Evaluation, Section of Cell Aging and Degeneration, Istituto Superiore di Sanita', Rome, Italy. 5 Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Fondazione Santa Lucia, Rome, Italy; Medical School, University Campus-Biomedico, Rome, Italy. 6 Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Fondazione Santa Lucia, Rome, Italy; Department of Experimental Medicine and Surgery, Division of Biochemistry, University of \"Tor Vergata\", Rome, Italy. 7 Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Fondazione Santa Lucia, Rome, Italy; Dulbecco Telethon Institute, Department of Biology, University of \"Tor Vergata\", Rome, Italy. 8 Department of Therapeutic Research and Medicine Evaluation, Section of Cell Aging and Degeneration, Istituto Superiore di Sanita', Rome, Italy; San Raffaele Institute, Sulmona, L'Aquila, Italy; Center of Integrated Metabolomics, Rome, Italy. 9 CNR - National Research Council, Cell Biology and Neurobiology Institute, Rome, Italy; Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Fondazione Santa Lucia, Rome, Italy. Electronic address: flaminia.pavone@cnr.it. (literal)
Titolo
  • Schwann cell autophagy counteracts the onset and chronification of neuropathic pain (literal)
Abstract
  • Axonal degeneration in peripheral nerves after injury is accompanied by myelin degradation initiated by Schwann cells (SCs). These cells activate autophagy, a ubiquitous cytoprotective process essential for degradation and recycling of cellular constituents. Concomitantly to nerve insult and axonal degeneration, neuropathic pain (NeP) arises. The role of SC autophagy in the mechanisms underlying NeP is still unknown. In this study, we examined the role of the autophagy during the early phase of Wallerian degeneration in NeP induction and chronification by using a murine model of peripheral nerve lesion (chronic constriction injury). We demonstrate that the autophagy inducer rapamycin, administered in the first week after nerve damage, induces long-lasting analgesic and antiinflammatory effects, facilitates nerve regeneration, and prevents pain chronification. Conversely, when autophagy is altered, by means of autophagic inhibitor 3-methyladenine administration or as occurs in activating molecule in Beclin-1-regulated autophagy transgenic mice (Ambra1(+/gt)), NeP is dramatically enhanced and prolonged. Immunohistochemical and ultrastructural evaluations show that rapamycin is able to increase autophagic flux in SCs, to accelerate myelin compaction, and to reduce inflammatory and immune reaction. Proteomic analysis combined with bioinformatic analysis suggests that a redox-sensitive mechanism could be responsible for SC autophagy activation. These data suggest that a deficiency of autophagic activity in SCs can be an early event in the origin of NeP chronification and that autophagy modulation may represent a powerful pharmacological approach to prevent the onset and chronification of NeP in the clinical setting. (literal)
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