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Título

NO and NOS isoforms in the development of apoptosis in renal ischemia/reperfusion

AutorViñas, Jose Luis CSIC ORCID; Solà, Anna M. CSIC ORCID; Genesca, Meritxell; Alfaro, Vicente; Pi, Felip CSIC; Hotter, Georgina CSIC ORCID
Palabras claveIschemia/reperfusion
Free radicals
Kidney
Nitric oxide
Nitric oxide synthase
Apoptosis
Fecha de publicación8-nov-2005
EditorElsevier
CitaciónFree Radical Biology and Medicine 40(6): 992-1003 (2006)
ResumenNitric oxide (NO) and the expression of endothelial (eNOS) and inducible (iNOS) isoforms of nitric oxide synthase (NOS) are recognized as important mediators of physiological and pathological processes of renal ischemia/reperfusion (I/R) injury, but little is known about their role in apoptosis. The ability of the eNOS/NO system to regulate the iNOS/NO system and thus promote apoptosis was assessed during experimental renal I/R. Renal caspase-3 activity and the number of TUNEL-positive cells increased with I/R, but decreased when NOS/NO systems were blocked with L-NIO (eNOS), 1400W (iNOS), and N-nitro-l-arginine methyl ester (L-NAME; a nonselective NOS inhibitor). I/R increased renal eNOS and iNOS expression as well as NO production. The NO increase was eNOS- and iNOS-dependent. Blockage of NOS/NO systems with L-NIO or L-NAME also resulted in a lower renal expression of iNOS and iNOS mRNA; in contrast, eNOS expression was not affected by iNOS-specific blockage. In conclusion, two pathways define the role of NOS/NO systems in the development of apoptosis during experimental renal I/R: a direct route, through eNOS overexpression and NO production, and an indirect route, through expression/activation of the iNOS/NO system, induced by eNOS. © 2005 Elsevier Inc. All rights reserved.
Versión del editorhttp://dx.doi.org/10.1016/j.freeradbiomed.2005.10.046
URIhttp://hdl.handle.net/10261/116496
DOI10.1016/j.freeradbiomed.2005.10.046
Identificadoresdoi: 10.1016/j.freeradbiomed.2005.10.046
issn: 0891-5849
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