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Overexpression of Human CD55 and CD59 or Treatment with Human CD55 Protects against Renal Ischemia-Reperfusion Injury in Mice.
Bongoni, Anjan K; Lu, Bo; Salvaris, Evelyn J; Roberts, Veena; Fang, Doreen; McRae, Jennifer L; Fisicaro, Nella; Dwyer, Karen M; Cowan, Peter J.
Afiliación
  • Bongoni AK; Immunology Research Centre, St. Vincent's Hospital Melbourne, Fitzroy, Victoria 3065, Australia.
  • Lu B; Immunology Research Centre, St. Vincent's Hospital Melbourne, Fitzroy, Victoria 3065, Australia.
  • Salvaris EJ; Immunology Research Centre, St. Vincent's Hospital Melbourne, Fitzroy, Victoria 3065, Australia.
  • Roberts V; Immunology Research Centre, St. Vincent's Hospital Melbourne, Fitzroy, Victoria 3065, Australia.
  • Fang D; Department of Medicine, University of Melbourne, Melbourne, Victoria 3065, Australia; and.
  • McRae JL; Immunology Research Centre, St. Vincent's Hospital Melbourne, Fitzroy, Victoria 3065, Australia.
  • Fisicaro N; Department of Medicine, University of Melbourne, Melbourne, Victoria 3065, Australia; and.
  • Dwyer KM; Immunology Research Centre, St. Vincent's Hospital Melbourne, Fitzroy, Victoria 3065, Australia.
  • Cowan PJ; Immunology Research Centre, St. Vincent's Hospital Melbourne, Fitzroy, Victoria 3065, Australia.
J Immunol ; 198(12): 4837-4845, 2017 06 15.
Article en En | MEDLINE | ID: mdl-28500075
Deficiency in the membrane-bound complement regulators CD55 and CD59 exacerbates renal ischemia-reperfusion injury (IRI) in mouse models, but the effect of increasing CD55 and CD59 activity has not been examined. In this study, we investigated the impact of overexpression of human (h) CD55 ± hCD59 or treatment with soluble rhCD55 in a mouse model of renal IRI. Unilaterally nephrectomised mice were subjected to 18 (mild IRI) or 22 min (moderate IRI) warm renal ischemia, and analyzed 24 h after reperfusion for renal function (serum creatinine and urea), complement deposition (C3b/c and C9), and infiltration of neutrophils and macrophages. Transgenic mice expressing hCD55 alone were protected against mild renal IRI, with reduced creatinine and urea levels compared with wild type littermates. However, the renal function of the hCD55 mice was not preserved in the moderate IRI model, despite a reduction in C3b/c and C9 deposition and innate cell infiltration. Mice expressing both hCD55 and hCD59, on the other hand, were protected in the moderate IRI model, with significant reductions in all parameters measured. Wild type mice treated with rhCD55 immediately after reperfusion were also protected in the moderate IRI model. Thus, manipulation of CD55 activity to increase inhibition of the C3 and C5 convertases is protective against renal IRI, and the additional expression of hCD59, which regulates the terminal complement pathway, provides further protection. Therefore, anti-complement therapy using complement regulatory proteins may provide a potential clinical option for preventing tissue and organ damage in renal IRI.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Daño por Reperfusión / Antígenos CD59 / Antígenos CD55 / Enfermedades Renales Tipo de estudio: Prognostic_studies Límite: Animals / Humans Idioma: En Revista: J Immunol Año: 2017 Tipo del documento: Article País de afiliación: Australia Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Daño por Reperfusión / Antígenos CD59 / Antígenos CD55 / Enfermedades Renales Tipo de estudio: Prognostic_studies Límite: Animals / Humans Idioma: En Revista: J Immunol Año: 2017 Tipo del documento: Article País de afiliación: Australia Pais de publicación: Estados Unidos