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Title

PGC-1α downregulation in steatotic liver enhances ischemia-reperfusion injury and impairs ischemic preconditioning

AuthorsSánchez-Ramos, Cristina; Prieto, Ignacio; Tierrez, Albert; Laso, Javier; Valdecantos, M. P.; Bartrons, Ramón; Roselló-Catafau, Joan ; Monsalve, María
KeywordsMitochondria
Oxidative metabolism
Antioxidants
Oxidative stress
Reactive oxygen species
Issue Date21-Jun-2017
CitationOCC World Congress (2017)
Annual SFRR-E Conference (2017)
AbstractLiver steatosis is associated with mitochondrial dysfunction and elevated Reactive Oxygen Species (ROS) levels together with enhanced sensitivity to IR injury and limited response to preconditioning protocols. Here, we sought to determine whether the downregulation in the steatotic liver of PGC-1a, a master regulator of mitochondrial metabolism and ROSl, could be responsible for the sensitivity of steatotic liver to ischemic damage. PGC-1a was induced in normal liver following exposure to an IR protocol concomitant with an increase in the levels of antioxidant proteins. By contrast, its induction was severely blunted in steatotic liver, resulting in a modest induction of antioxidant proteins. Livers of PGC-1a-/- mice on chow diet were normal, but they exhibited an enhanced sensitivity to IR injury and also a lack of response to ischemic preconditioning, a phenotype that recapitulated the features of steatotic liver in terms of liver damage. Utilizing an in vitro model of IPC, we found that PGC-1a expression was downregulated in hepatic cells cultured at 1% O2 whereas it was induced following reoxygenation (3% O2), and was responsible for the recovery of antioxidant gene expression following the ischemic period. We concluded that PGC-1a plays an important role in the protection against IR injury in the liver, which is likely associated with its capacity to induce antioxidant gene expression.
DescriptionTrabajo presentado en el OCC World Congress / Annual SFRR-E Conference: Metabolic Stress and Redox Regulation, celebrado en Berlín, Alemania, del 21 al 23 de junio de 2017
Publisher version (URL)https://doi.org/10.1016/j.freeradbiomed.2017.04.143
URIhttp://hdl.handle.net/10261/177688
DOIhttp://dx.doi.org/10.1016/j.freeradbiomed.2017.04.143
Appears in Collections:(IIBB) Comunicaciones congresos
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