Bringing PGE2 in from the cold

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Science  12 Jun 2015:
Vol. 348, Issue 6240, pp. 1208-1209
DOI: 10.1126/science.aac5515

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Prostaglandins (PGs) are evanescent, locally acting lipids. They are not stored within cells, but are generated when their precursor, arachidonic acid, is mobilized from cellular membranes by rather nonspecific activation of phospholipases. Most cells generate one or two dominant PGs, each with a remarkable diversity of effects. Prostaglandin E2 (PGE2) is a vasodilator that acts with other PGs and metabolic products of arachidonic acid to promote pain and inflammation. The development and clinical use of drugs that suppress the production of these PGs has been ongoing for decades, but PGE2 also has been long recognized to have a role in tissue maintenance and regeneration. Its stable analog, dimethyl PGE2, is currently being evaluated for use as an adjunct to hematopoietic stem cell transplantation. On page 1223 of this issue, Zhang et al. (1) report that elevating the capacity of tissues to form PGE2 by inhibiting 15-hydroxyprostaglandin dehydrogenase (15-PGDH), its major inactivating enzyme, augments the capacity for tissue regeneration in mouse models. So, is it time to bring PGE2, which we are so used to suppressing, in from the cold?