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dc.contributor.CRUESPUNIVERSIDADE DE ESTADUAL DE CAMPINASpt_BR
dc.typeArtigo de Periódicopt_BR
dc.titleImpairment Of Toll-like Receptors 2 And 4 Leads To Compensatory Mechanisms After Sciatic Nerve Axotomypt_BR
dc.contributor.authorFreriapt_BR
dc.contributor.authorCM; Bernardespt_BR
dc.contributor.authorD; Almeidapt_BR
dc.contributor.authorGL; Simoespt_BR
dc.contributor.authorGF; Barbosapt_BR
dc.contributor.authorGO; Oliveirapt_BR
dc.contributor.authorALRpt_BR
unicamp.author.emailalroliv@unicamp.brpt_BR
dc.subjectPheripheral Nerve Injurypt_BR
dc.subjectAxotomypt_BR
dc.subjectToll-like Receptors And Functional Recoverypt_BR
dc.description.abstractPeripheral nerve injury results in retrograde cell body-related changes in the spinal motoneurons that will contribute to the regenerative response of their axons. Successful functional recovery also depends on molecular events mediated by innate immune response during Wallerian degeneration in the nerve microenvironment. A previous study in our lab demonstrated that TLR 2 and 4 develop opposite effects on synaptic stability in the spinal cord after peripheral nerve injury. Therefore, we suggested that the better preservation of spinal cord microenvironment would positively influence distal axonal regrowth. In this context, the present work aimed to investigate the influence of TLR2 and TLR4 on regeneration and functional recovery after peripheral nerve injury. Methods: Eighty-eight mice were anesthetized and subjected to unilateral sciatic nerve crush (C3H/HeJ, n = 22, C3H/HePas, n = 22; C57Bl6/J, n = 22 and TLR2(-/-), n = 22). After the appropriate survival times (3, 7, 14 days, and 5 weeks), all mice were killed and the sciatic nerves and tibialis cranialis muscles were processed for immunohistochemistry and transmission electron microscopy (TEM). Gait analysis, after sciatic nerve crushing, was performed in another set of mice (minimum of n = 8 per group), by using the walking track test (CatWalk system). Results: TLR4 mutant mice presented greater functional recovery as well as an enhanced p75(NTR) and neurofilament protein expression as compared to the wild-type strain. Moreover, the better functional recovery in mutant mice was correlated to a greater number of nerve terminal sprouts. Knockout mice for TLR2 exhibited 30 % greater number of degenerated axons in the distal stump of the sciatic nerve and a decreased p75NTR and neurofilament protein expression compared to the wild type. However, the absence of TLR2 receptor did not influence the overall functional recovery. End-point equivalent functional recovery in transgenic mice may be a result of enhanced axonal diameter found at 2 weeks after lesion. Conclusions: Altogether, the present results indicate that the lack of TLR2 or the absence of functional TLR4 does affect the nerve regeneration process; however, such changes are minimized through different compensatory mechanisms, resulting in similar motor function recovery, as compared to wild-type mice. These findings contribute to the concept that innate immune-related molecules influence peripheral nerve regeneration by concurrently participating in processes taking place both at the CNS and PNS.en
dc.relation.ispartofJournal of Neuroinflammationpt_BR
dc.publisher.cityLONDONpt_BR
dc.publisherBIOMED CENTRAL LTDpt_BR
dc.date.issued2016pt_BR
dc.identifier.citationJournal Of Neuroinflammation. BIOMED CENTRAL LTD, n. 13, n. 118, p. .pt_BR
dc.language.isoEnglishpt_BR
dc.description.volume13pt_BR
dc.description.issuenumberpt_BR
dc.description.lastpagept_BR
dc.rightsabertopt_BR
dc.sourceWOSpt_BR
dc.identifier.issn1742-2094pt_BR
dc.identifier.wosidWOS:000377286500003pt_BR
dc.identifier.doi10.1186/s12974-016-0579-6pt_BR
dc.identifier.urlhttp://jneuroinflammation.biomedcentral.com.ez88.periodicos.capes.gov.br/articles/10.1186/s12974-016-0579-6pt_BR
dc.description.sponsorshipFapesp [2010/17688-7, 2009/50307-0, 2015/04665-2, 2010/07476-2]pt_BR
dc.description.sponsorshipCNPq (Brazil)pt_BR
dc.description.sponsorship1Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt_BR
dc.description.sponsorship1Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)pt_BR
dc.date.available2016-12-06T18:31:59Z-
dc.date.accessioned2016-12-06T18:31:59Z-
dc.description.provenanceMade available in DSpace on 2016-12-06T18:31:59Z (GMT). No. of bitstreams: 1 000377286500003.pdf: 4262270 bytes, checksum: 6232eb887cd3807569ccafd0dfe18bd4 (MD5) Previous issue date: 2016en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/320424-
dc.description.conferencelocationpt_BR
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