Brasil | Artículos de revistas
dc.creatorSEMEDO, Patricia
dc.creatorDONIZETTI-OLIVEIRA, Cassiano
dc.creatorBURGOS-SILVA, Marina
dc.creatorCENEDEZE, Marco Antonio
dc.creatorMALHEIROS, Denise Maria Avancini Costa
dc.creatorPACHECO-SILVA, Alvaro
dc.creatorCAMARA, Niels Olsen Saraiva
dc.date.accessioned2012-10-20T03:22:29Z
dc.date.accessioned2018-07-04T15:35:43Z
dc.date.available2012-10-20T03:22:29Z
dc.date.available2018-07-04T15:35:43Z
dc.date.created2012-10-20T03:22:29Z
dc.date.issued2010
dc.identifierLABORATORY INVESTIGATION, v.90, n.5, p.685-695, 2010
dc.identifier0023-6837
dc.identifierhttp://producao.usp.br/handle/BDPI/28270
dc.identifier10.1038/labinvest.2010.45
dc.identifierhttp://dx.doi.org/10.1038/labinvest.2010.45
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1624913
dc.description.abstractOne of the early phases that lead to fibrosis progression is inflammation. Once this stage is resolved, fibrosis might be prevented. Bone marrow mononuclear cells (BMMCs) are emerging as a new therapy for several pathologies, including autoimmune diseases, because they enact immunosuppression. In this study we aimed to evaluate the role of BMMC administration in a model of kidney fibrosis induced by an acute injury. C57Bl6 mice were subjected to unilateral severe ischemia by clamping the left renal pedicle for 1 h. BMMCs were isolated from femurs and tibia, and after 6 h of reperfusion, 1 x 10(6) cells were administrated intraperitoneally. At 24 h after surgery, treated animals showed a significant decrease in creatinine and urea levels when compared with untreated animals. Different administration routes were tested. Moreover, interferon (IFN) receptor knockout BMMCs were used, as this receptor is necessary for BMMC activation. Labeled BMMCs were found in ischemic kidney on FACS analysis. This improved outcome was associated with modulation of inflammation in the kidney and systemic modulation, as determined by cytokine expression profiling. Despite non-amelioration of functional parameters, kidney mRNA expression of interleukin (IL)-6 at 6 weeks was lower in BMMC-treated animals, as were levels of collagen 1, connective tissue growth factor (CTGF), transforming growth factor-beta (TGF-beta) and vimentin. Protective molecules, such as IL-10, heme oxygenase 1 (HO-1) and bone morphogenetic 7 (BMP-7), were increased in treated animals after 6 weeks. Moreover, Masson and Picrosirius red staining analyses showed less fibrotic areas in the kidneys of treated animals. Thus, early modulation of inflammation by BMMCs after an ischemic injury leads to reduced fibrosis through modulation of early inflammation.
dc.languageeng
dc.publisherNATURE PUBLISHING GROUP
dc.relationLaboratory Investigation
dc.rightsCopyright NATURE PUBLISHING GROUP
dc.rightsrestrictedAccess
dc.subjectmesenchymal stem cell
dc.subjectacute kidney injury
dc.subjectischemia-reperfusion injury
dc.subjectfibrosis
dc.subjectinflammation
dc.subjectbone marrow
dc.titleBone marrow mononuclear cells attenuate fibrosis development after severe acute kidney injury
dc.typeArtículos de revistas


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