Proteolytic processed form of CXCL12 abolishes migration and induces apoptosis in neural stem cells in vitro

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dc.citation.volume22]
dc.contributor.authorAdelita, Tais [UNIFESP]
dc.contributor.authorStilhano, Roberta Sessa [UNIFESP]
dc.contributor.authorHan, SangWon [UNIFESP]
dc.contributor.authorJusto, Giselle Zenker [UNIFESP]
dc.contributor.authorPorcionatto, Marimelia [UNIFESP]
dc.coverageAmsterdam
dc.date.accessioned2020-06-26T16:30:30Z
dc.date.available2020-06-26T16:30:30Z
dc.date.issued2017
dc.description.abstractThe subventricular zone (SVZ) of the adult mammalian brain hosts full potential neural stem cells (NSCs). NSCs are able to respond to extracellular signals in the brain, amplifying the pool of progenitor cells and giving rise to neuroblasts that showability to migrate towards an injury site. These signals can come fromvascular system, cerebrospinal fluid, glial cells, or projections of neurons in adjoining regions. CXCL12, a chemokine secreted after brain injury, reaches the SVZ in a gradient manner and drives neuroblasts towards the lesion area. Among many other molecules, matrix metalloproteinase 2 and 9 (MMP-2/9) are also released during brain injury. MMP-2/9 can cleave CXCL12 generating a new molecule, CXCL12(5-67), and its effects on NSCs viability is not well described. Here we produced recombinant CXCL12 and CXCL12(5-67) and evaluated their effect inmurine adultNSCsmigration and survival in vitro. We showed CXCL12(5-67) does not promote NSCsmigration, but does induce cell death. The NSC death induced by CXCL12(5-67) involves caspases 9 and 3/7 activation, implying the intrinsic apoptotic pathway in this phenomenon. Our evidences in vitromake CXCL12(5-67) and its receptor potential candidates for brain injuries and neurodegeneration studies. (C) 2017 The Author(s). Published by Elsevier B.V.en
dc.description.affiliationUniv Fed Sao Paulo, Escola Paulista Med, Dept Biochem, BR-04039 Sao Paulo, Brazil
dc.description.affiliationUniv Fed Sao Paulo, Escola Paulista Med, Dept Biophys, BR-04044 Sao Paulo, Brazil
dc.description.affiliationUniv Fed Sao Paulo, Dept Cell Biol, BR-09920 Diadema, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Escola Paulista Med, Dept Biochem, BR-04039 Sao Paulo, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Escola Paulista Med, Dept Biophys, BR-04044 Sao Paulo, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Dept Cell Biol, BR-09920 Diadema, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFAPESP
dc.description.sponsorshipCNPq
dc.description.sponsorshipIDFAPESP: 2011/11388-4
dc.description.sponsorshipIDFAPESP: 2012/00652-5
dc.description.sponsorshipIDFAPESP: 2015/19231-8
dc.description.sponsorshipIDCNPq: 404646/2012-3
dc.format.extent61-69
dc.identifierhttp://dx.doi.org/10.1016/j.scr.2017.05.013]
dc.identifier.citationStem Cell Research. Amsterdam, v. 22, p. 61-69, 2017.
dc.identifier.doi10.1016/j.scr.2017.05.013
dc.identifier.fileWOS000405469000009.pdf
dc.identifier.issn1873-5061
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/53576
dc.identifier.wosWOS:000405469000009
dc.language.isoeng
dc.publisherElsevier Science Bv
dc.relation.ispartofStem Cell Research
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectCXCL12en
dc.subjectCXCL12(5-67)en
dc.subjectAdult neural stem cellen
dc.subjectMigrationen
dc.subjectApoptosisen
dc.subjectIn vitro studyen
dc.titleProteolytic processed form of CXCL12 abolishes migration and induces apoptosis in neural stem cells in vitroen
dc.typeinfo:eu-repo/semantics/article
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