Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/348884
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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampBeraldo, Felipe Caetano-
dc.contributor.authorunicampMazzali, Marilda-
dc.typeArtigopt_BR
dc.titleAdministration of neural precursor cells ameliorates renal ischemia-reperfusion injurypt_BR
dc.contributor.authorWang, P.H.M-
dc.contributor.authorSchwindt, T.T.-
dc.contributor.authorBarnabé, G.F.-
dc.contributor.authorMotta, F.L.T.-
dc.contributor.authorSemedo, P.-
dc.contributor.authorBeraldo, F.C.-
dc.contributor.authorMazzali, M.-
dc.contributor.authordos Reis, M.A.-
dc.contributor.authorTeixeira, V.P.-
dc.contributor.authorPacheco-Silva, A.-
dc.contributor.authorMello, L.E.-
dc.contributor.authorCâmara, N.O.S.-
dc.subjectCélulaspt_BR
dc.subjectReperfusãopt_BR
dc.subject.otherlanguageCellspt_BR
dc.subject.otherlanguageReperfusionpt_BR
dc.description.abstractIn this study we evaluated whether administration of stem cells of neural origin (neural precursor cells, NPCs) could be protective against renal ischemia-reperfusion injury (IRI). We hypothesized that stem cell outcomes are not tissue-specific and that NPCs can improve tissue damage through paracrine mechanisms, especially due to immunomodulation. To this end, Wistar rats (200–250 g) were submitted to 1-hour ischemia and treated with NPCs (4 × 106 cells/animal) at 4 h of reperfusion. To serve as controls, ischemic animals were treated with cerebellum homogenate harvested from adult rat brain. All groups were sacrificed at 24 h of reperfusion. NPCs were isolated from rat fetus telencephalon and cultured until neurosphere formation (7 days). Before administration, NPCs were labeled with carboxyfluorescein diacetate succinimydylester (CFSE). Kidneys were harvested for analysis of cytokine profile and macrophage infiltration. At 24 h, NPC treatment resulted in a significant reduction in serum creatinine (IRI + NPC 1.21 + 0.18 vs. IRI 3.33 + 0.14 and IRI + cerebellum 2.95 + 0.78mg/dl, p < 0.05) and acute tubular necrosis (IRI + NPC 46.0 + 2.4% vs. IRI 79.7 + 14.2%, p < 0.05). NPC-CFSE and glial fibrillary acidic protein (GFAP)-positive cells (astrocyte marker) were found exclusively in renal parenchyma, which also presented GFAP and SOX-2 (an embryonic neural stem cell marker) mRNA expression. NPC treatment resulted in lower renal proinflammatory IL1-β and TNF-α expression and higher anti-inflammatory IL-4 and IL-10 transcription. NPC-treated animals also had less macrophage infiltration and decreased serum proinflammatory cytokines (IL-1β, TNF-α and INF-γ). Our data suggested that NPC therapy improved renal function by influencing immunological responsespt_BR
dc.relation.ispartofNephron experimental nephrologypt_BR
dc.publisher.cityBaselpt_BR
dc.publisher.countrySuíçapt_BR
dc.publisherS. Kargerpt_BR
dc.date.issued2009-
dc.language.isoengpt_BR
dc.description.volume112pt_BR
dc.description.issuenumber1pt_BR
dc.description.firstpagee20pt_BR
dc.description.lastpagee28pt_BR
dc.rightsFechadopt_BR
dc.sourceWOSpt_BR
dc.identifier.issn1660-2129pt_BR
dc.identifier.eissn1660-2129pt_BR
dc.identifier.doi10.1159/000210575pt_BR
dc.identifier.urlhttps://www.karger.com/Article/FullText/210575pt_BR
dc.description.sponsorshipFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESPpt_BR
dc.description.sponsordocumentnumber04/08311-6; 04/13826-5; 05/50085-6; 07/07139-3pt_BR
dc.date.available2020-09-08T19:32:05Z-
dc.date.accessioned2020-09-08T19:32:05Z-
dc.description.provenanceSubmitted by Susilene Barbosa da Silva (susilene@unicamp.br) on 2020-09-08T19:32:05Z No. of bitstreams: 0. Added 1 bitstream(s) on 2021-01-04T15:12:56Z : No. of bitstreams: 1 000265628600003.pdf: 484840 bytes, checksum: 93e907e6eea450a414918f34e5c58ed7 (MD5)en
dc.description.provenanceMade available in DSpace on 2020-09-08T19:32:05Z (GMT). No. of bitstreams: 0 Previous issue date: 2009en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/348884-
dc.contributor.departmentSem informaçãopt_BR
dc.contributor.departmentDepartamento de Clínica Médicapt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.subject.keywordIschemiapt_BR
dc.identifier.source000265628600003pt_BR
dc.creator.orcidSem informaçãopt_BR
dc.creator.orcid0000-0001-6297-4909pt_BR
dc.type.formArtigo originalpt_BR
dc.description.sponsorNoteThis work was supported by MCT/CT-Saúde/Decit/SCTIE/MS, grant No. 552307/2005-0, and Fundação de Apoio à Pesquisa do Estado de São Paulo, grant Nos. 04/08311-6, 04/13826-5, 05/50085-6 and 07/07139-3pt_BR
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