Adrenic acid (AA), the 2-carbon elongation product of arachidonic acid, is present at significant levels in membrane phospholipids of mouse peritoneal macrophages. Despite its abundance and structural similarity to arachidonic acid, very little is known about the molecular mechanisms governing adrenic acid mobilization in cells of the innate immune system. This contrasts with the wide availability of data on arachidonic acid mobilization. In this work, we used mass-spectrometry-based lipidomic procedures to define the profiles of macrophage phospholipids that contain adrenic acid and their behavior during receptor activation. We identified the phospholipid sources from which adrenic acid is mobilized, and compared the data with arachidonic acid mobilization. Taking advantage of the use of selective inhibitors, we also showed that cytosolic group IVA phospholipase A2 is involved in the release of both adrenic and arachidonic acids. Importantly, calcium independent group VIA phospholipase A2 spared arachidonate-containing phospholipids and hydrolyzed only those that contain adrenic acid. These results identify separate mechanisms for regulating the utilization of adrenic and arachidonic acids, and suggest that the two fatty acids may serve non-redundant functions in cells.

La displasia fibrosa (DF) es una enfermedad fibroósea benigna que consiste en el reemplazamiento de hueso normal con excesiva proliferación de tejido conectivo fibroso con estructuras óseas afuncionales. La forma de DF craneofacial es poco frecuente y no está bien definida. La afectación más frecuente en el área craneofacial se da en el cuerpo de la mandíbula y zona posterior del maxilar. Los autores describen el manejo completo y la rehabilitación funcional de un caso de displasia fibrosa de mandíbula avanzado y revisan las opciones terapéuticas de esta condición.