Assessment of a dual regulatory role for NO in liver regeneration after partial hepatectomy: protection against apoptosis and retardation of hepatocyte proliferation.
FASEB J
; 19(8): 995-7, 2005 Jun.
Article
en En
| MEDLINE
| ID: mdl-15788446
ABSTRACT
The role of hepatic nitric oxide (NO) in liver regeneration after partial hepatectomy (PH) was studied in animals carrying a nitric oxide synthase-2 transgene under the control of the phospho(enol)pyruvate carboxykinase promoter. These mice expressed NOS-2 in liver cells under fasting conditions. Liver mass recovery and molecular parameters related to cell proliferation were determined after PH. Preexisting hepatic NO synthesis, as well as NO delivery by NO-donors, impaired early signaling (for example, attenuated NF-kappaB activation and TNF-alpha and IL-6 release). The regenerative process was also impaired as a result of an insufficient proliferative response, but mouse survival after surgery was not compromised. However, NO exerted a protective role against apoptosis in transgenic hepatectomized mice. Local production of NO in liver cells, achieved by hydrodynamic-based transfection with a NOS-2-encoding plasmid, also resulted in delayed liver recovery after PH and also protected against Fas-mediated apoptosis. These data show that sustained presence of NO after PH exerts a dual role attenuating liver regeneration while efficiently protecting against liver apoptosis.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Apoptosis
/
Hepatocitos
/
Hepatectomía
/
Regeneración Hepática
/
Óxido Nítrico
Límite:
Animals
Idioma:
En
Revista:
FASEB J
Asunto de la revista:
BIOLOGIA
/
FISIOLOGIA
Año:
2005
Tipo del documento:
Article