Role of caspases on cell death, inflammation, and cell cycle in glycerol-induced acute renal failure

dc.creatorHomsi, E
dc.creatorJanino, P
dc.creatorde Faria, JBL
dc.date2006
dc.dateAPR
dc.date2014-11-17T18:25:30Z
dc.date2015-11-26T17:41:16Z
dc.date2014-11-17T18:25:30Z
dc.date2015-11-26T17:41:16Z
dc.date.accessioned2018-03-29T00:23:03Z
dc.date.available2018-03-29T00:23:03Z
dc.identifierKidney International. Nature Publishing Group, v. 69, n. 8, n. 1385, n. 1392, 2006.
dc.identifier0085-2538
dc.identifierWOS:000237008600019
dc.identifier10.1038/sj.ki.5000315
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/71208
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/71208
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/71208
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1286963
dc.descriptionCaspases are the main executioners of apoptosis as well as interleukin (IL)-1 beta and IL-18 conversion to active forms. They are activated after acute kidney injuries. In this study, we evaluated the importance of the caspase family in the pathogenesis and recovery of glycerol-induced acute renal failure in rats (Gly-ARF). Rats were treated with pan-caspase or selective caspase 1 and 3 inhibitors at the moment we injected glycerol. Renal function, renal histology ( HE), transferase- mediated deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling staining for apoptosis, leukocytes infiltration ( immunohistochemistry), renal expression of IL-1 beta and IL-18 ( immunohistochemistry and Western blot), tubular regeneration ( 5-bromo-2'-deoxyuridine ( BrdU) incorporation), and P27(Kip) expression ( Western blot) were evaluated at appropriate times. All inhibitors reduced the renal function impairment. Pan-caspase and caspase-3 inhibitors reduced cellular death ( necrosis and apoptosis) 24 h after Gly-ARF. All caspases inhibitors reduced macrophages infiltration. The expression of total IL-1 beta was enhanced in Gly-ARF, but the active IL-1 beta and IL-18 forms were abolished in pan-caspase treated rats. Caspase-1 inhibitor attenuated Gly-ARF but not tubular injury suggesting glomerular hemodynamic improvement. There was striking regenerative response 48 h after Gly-ARF characterized by enhanced BrdU incorporation and reduced expression of p27(Kip.) This response was not blunted by caspases inhibition. Our findings demonstrate that caspases participate in important pathogenic mechanisms in Gly-ARF such as inflammation, apoptosis, vasoconstriction, and tubular necrosis. The early inhibition of caspases attenuates these mechanisms and reduces the renal function impairment in Gly-ARF.
dc.description69
dc.description8
dc.description1385
dc.description1392
dc.languageen
dc.publisherNature Publishing Group
dc.publisherNew York
dc.publisherEUA
dc.relationKidney International
dc.relationKidney Int.
dc.rightsfechado
dc.sourceWeb of Science
dc.subjectacute renal failure
dc.subjectapoptosis
dc.subjectinflammation
dc.subjectcaspases
dc.subjectAcute Tubular-necrosis
dc.subjectCaspase-1-deficient Mice
dc.subjectIschemia-reperfusion
dc.subjectGlomerular Hemodynamics
dc.subjectInduced Apoptosis
dc.subjectBlood-flow
dc.subjectInjury
dc.subjectActivation
dc.subjectRat
dc.subjectInhibition
dc.titleRole of caspases on cell death, inflammation, and cell cycle in glycerol-induced acute renal failure
dc.typeArtículos de revistas


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