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During 2013 we have focused on studying the role of cyclooxygenase 2 (COX-2)
Highlights
after liver damage, either in situations of hepatocellular carcinoma (HCC) or in

situations of hyperglycemia. In these cases we found that while the COX-2 has no
implications on liver tumor progression, overexpression of COX-2 protects the he-

patocyte against apoptosis induced by hyperglycemia in type 1 diabetes models.

We have completed the study with other enzymes in the pathway of synthesis and
degradation of prostaglandins, suggesting that the 15 -hydroxyprostaglandina de-

hydrogenase (15-PGDH) could function as a relevant tumor suppressor in HCC.

On the other hand, our group has also focused its work on studying the role of ma-

crophages in the pathophysiology of major organs. In 2013, we have highlighted
that prostaglandin E2 (PGE2) selectively impairs pyrimidine receptors P2Y Ca2+

mobilization. This inhibition involves the activation of nPKCs and PKD, providing
new clues to understand the resolution phase of inflammation, when accumulation

of PGE2 anti-inflammatory and proresolving mediators occurs. We have also pro-

vided evidence for a new mechanism by which the 15 -epi- lipoxin 4 contributes
to inflammation resolution, consisting of the reversion of LPS effects on voltage-

dependent potassium channels Kv and Kir in macrophages.

Finally, we have characterized a new variant of the 6-fosfofructo-2-quinasa/fructo-

sa-2,6-bisphosphatase in fetal liver that controls the atypical regulation of glucose
metabolism in this stage of development.

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