FTY720 impairs necrosis development after ischemia-reperfusion injury

FTY720 impairs necrosis development after ischemia-reperfusion injury

Autor Oliveira, CMS Google Scholar
Borra, R. C. Google Scholar
Franco, M. Google Scholar
Schor, N. Google Scholar
Silva, H. T. Google Scholar
Pestana, JOM Google Scholar
Bueno, V Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Resumo Ischemia-reperfusion (IR) injury is a common early feature that contributes to graft damage by impairing resident cell function. Our previous results showed that IR injury impaired renal function, by causing extensive tubular necrosis and increasing MHC class II and ICAM-1 molecule expression by mesangial cells (MC). MCs are likely candidates to come into close contact with immune cells such as monocytes or lymphocytes. It has been suggested that under inflammatory circumstances, there is increased MC expression of MHC class II, of adhesion molecules (such as ICAM-1), of cytokines receptors, and of molecules associated with cellular death (apoptosis). the immunosuppressive properties of FTY720 have been shown in clinical and experimental situations. It has also been shown to be protective against IR injury in rats. We sought to evaluate the role of FTY720 in a murine IR model by measuring renal function, tubular necrosis, and surface molecule expression by cultured mesangial cells. Intravenous administration of FTY720 (1 mg/kg) immediately before IR induction did not improve the short-term (24 hours) outcome of renal function or reduced MHC class II and ICAM-1 surface molecule expression. However, there was a decreased percentage of tubular necrosis in mice treated with FTY720 (51.3% +/- 1.6%) compared with vehicle-treated mice (66% +/- 5.5%). These results suggest a protective role of FTY720 in an IR injury model. More studies are required to identify the mechanisms involved in the protective activity of FTY720 in the IR injury model.
Idioma Inglês
Data 2004-05-01
Publicado em Transplantation Proceedings. New York: Elsevier B.V., v. 36, n. 4, p. 854-856, 2004.
ISSN 0041-1345 (Sherpa/Romeo, fator de impacto)
Editor Elsevier B.V.
Extensão 854-856
Fonte http://dx.doi.org/10.1016/j.transproceed.2004.03.045
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000222063800017
URI http://repositorio.unifesp.br/handle/11600/27736

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