{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,24]],"date-time":"2026-01-24T07:57:58Z","timestamp":1769241478573,"version":"3.49.0"},"reference-count":44,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2013,2,14]],"date-time":"2013-02-14T00:00:00Z","timestamp":1360800000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Eur J of Neuroscience"],"published-print":{"date-parts":[[2013,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Wallerian degeneration (<jats:styled-content style=\"fixed-case\">WD<\/jats:styled-content>) comprises a series of events that includes activation of non\u2010neuronal cells and recruitment of immune cells, creating an inflammatory milieu that leads to extensive nerve fragmentation and subsequent clearance of the myelin debris, both of which are necessary prerequisites for effective nerve regeneration. Previously, we documented accelerated axon regeneration in animals lacking galectin\u20103 (<jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>al\u20103), a molecule associated with myelin clearance. To clarify the mechanisms underlying this enhanced regeneration, we focus here on the early steps of <jats:styled-content style=\"fixed-case\">WD<\/jats:styled-content> following sciatic nerve crush in <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>al\u20103<jats:sup>\u2212\/\u2212<\/jats:sup> mice. Using an <jats:italic>in vivo<\/jats:italic> model of nerve degeneration, we observed that removal of myelin debris is more efficient in <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>al\u20103<jats:sup>\u2212\/\u2212<\/jats:sup> than in wild\u2010type (<jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content>) mice; we next used an <jats:italic>in vitro<\/jats:italic> phagocytosis assay to document that the phagocytic potential of macrophages and <jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>chwann cells was enhanced in the <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>al\u20103<jats:sup>\u2212\/\u2212<\/jats:sup> mice. Moreover, both <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> and protein levels for the pro\u2010inflammatory cytokines <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2 and <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010\u03b1, as well as for <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>oll\u2010like receptor (<jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>)\u20102 and \u20104, show robust increases in injured nerves from <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>al\u20103<jats:sup>\u2212\/\u2212<\/jats:sup>mice compared to those from <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> mice. Collectively, these data indicate that the lack of <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>al\u20103 results in an augmented inflammatory profile that involves the <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>\u2013cytokine pathway, and increases the phagocytic capacity of Schwann cells and macrophages, which ultimately contributes to speeding the course of <jats:styled-content style=\"fixed-case\">WD<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/ejn.12161","type":"journal-article","created":{"date-parts":[[2013,2,14]],"date-time":"2013-02-14T07:44:45Z","timestamp":1360827885000},"page":"1682-1690","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":39,"title":["Lack of galectin\u20103 speeds <scp>W<\/scp>allerian degeneration by altering <scp>TLR<\/scp> and pro\u2010inflammatory cytokine expressions in injured sciatic nerve"],"prefix":"10.1111","volume":"37","author":[{"given":"Bruno Siqueira","family":"Mietto","sequence":"first","affiliation":[{"name":"Laborat\u00f3rio de Neurodegenera\u00e7\u00e3o e Reparo Programa de Pesquisa em Neuroci\u00eancia B\u00e1sica e Cl\u00ednica Instituto de Ci\u00eancias Biom\u00e9dicas Universidade Federal do Rio de Janeiro Rio de Janeiro RJ Brazil"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sofia","family":"Jurgensen","sequence":"additional","affiliation":[{"name":"Laborat\u00f3rio de Neurodegenera\u00e7\u00e3o e Reparo Programa de Pesquisa em Neuroci\u00eancia B\u00e1sica e Cl\u00ednica Instituto de Ci\u00eancias Biom\u00e9dicas Universidade Federal do Rio de Janeiro Rio de Janeiro RJ Brazil"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lucin\u00e9ia","family":"Alves","sequence":"additional","affiliation":[{"name":"Laborat\u00f3rio de Neurodegenera\u00e7\u00e3o e Reparo Programa de Pesquisa em Neuroci\u00eancia B\u00e1sica e Cl\u00ednica Instituto de Ci\u00eancias Biom\u00e9dicas Universidade Federal do Rio de Janeiro Rio de Janeiro RJ Brazil"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cyntia","family":"Pecli","sequence":"additional","affiliation":[{"name":"Laborat\u00f3rio de Imunofarmacologia Instituto de Ci\u00eancias Biom\u00e9dicas Universidade Federal do Rio de Janeiro Rio de Janeiro RJ Brazil"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marcelo Sampaio","family":"Narciso","sequence":"additional","affiliation":[{"name":"Laborat\u00f3rio de Neurodegenera\u00e7\u00e3o e Reparo Programa de Pesquisa em Neuroci\u00eancia B\u00e1sica e Cl\u00ednica Instituto de Ci\u00eancias Biom\u00e9dicas Universidade Federal do Rio de Janeiro Rio de Janeiro RJ Brazil"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Iranaia","family":"Assun\u00e7\u00e3o\u2010Miranda","sequence":"additional","affiliation":[{"name":"Laborat\u00f3rio de Resposta Celular \u00e1 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