Page 97 - CIBEREHD2016-ENG
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Most relevant scientific articles
• Motino O., Agra N., Brea Contreras R., Dominguez-Moreno M., Garcia-Monzon C., Vargas- Castrillon J. et al. Cyclooxygenase-2 expression in hepatocytes attenuates non-alcoholic steatohepatitis and liver fibrosis in mice. Biochimica et Biophysica Acta - Molecular Basis of Disease. 2016;1862(9):1710-1723.
• Singh P., Gonzalez-Ramos S., Mojena M., Rosales-Mendoza C.E., Emami H., Swanson J. et al. GM- CSF Enhances macrophage glycolytic activity in vitro and improves detection of inflammation in vivo. Journal of Nuclear Medicine. 2016;57(9):1428-1435.
• Klionsky DJ, Abdelmohsen K, Abe A, Abedin MJ, Abeliovich H, Acevedo Arozena A et al. Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition). Autophagy. 2016;12(1):1-222.
Hightlights
During 2016 we have focused on studying the contribution of cyclooxygenase-2-dependent prostaglandins to the pathogenesis of steatohepatitis and hepatic fibrosis in collaboration with Carmelo García-Monzón from Ciberehd and Ángela Valverde from Ciberdem. Our study demonstrated that, hCOX-2-Tg mice
fed MCD diet showed lower grades of steatosis, ballooning and inflammation than Wt mice, in part by reduced recruitment and infiltration of hepatic macrophages, with a corresponding decrease in serum levels of pro-inflammatory cytokines. Furthermore, hCOX-2-Tg mice showed a significant attenuation of the MCD diet-induced increase in oxidative stress and hepatic apoptosis observed in Wt mice. Even more, hCOX-2-Tg mice treated with CCl4 had significantly lower stages of fibrosis and less hepatic content of collagen, hydroxyproline and pro-fibrogenic markers than Wt controls. Collectively, our data indicates that constitutive hepatocyte COX-2 expression ameliorates NASH and liver fibrosis development in mice by reducing inflammation, oxidative stress and apoptosis and by modulating activation of hepatic stellate cells, respectively, suggesting a possible protective role for COX-2 induction in NASH/NAFLD progression. In collaboration with Lisardo Boscá we have studied the effect of granulocyte-macrophage colony- stimulating factor (GM-CSF), a clinically used cytokine in the glycolytic activity of macrophages and
the conclusion is that GM-CSF augments glycolytic flux in vitro and increases 18F-FDG uptake within inflamed atheroma in vivo. These findings demonstrate that GM-CSF can be used to enhance detection of inflammation.
In this year we have got a new Project from MINECO “Role of COX-2 in hepatic ischemia/reperfusion injury. Study of mitochondrial function” (2017-19).
EHD
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