2024-03-28T20:42:23Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/246802021-10-27T12:01:39Zcom_10261_22com_10261_1col_10261_275
Zeini, Miriam
Hortelano, Sonsoles
Través, Paqui G.
Boscá, Lisardo
2010-05-25T13:05:39Z
2010-05-25T13:05:39Z
2005-06
Faseb Journal 19(8): 995-997 (2005)
0892-6638
http://hdl.handle.net/10261/24680
10.1096/fj.04-3233fje
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.
eng
closedAccess
Nitric oxide synthase
Transgenic
Gene therapy
Assessment of a dual regulatory role for NO in liver regeneration after partial hepatectomy: protection against apoptosis and retardation of hepatocyte proliferation
artículo