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20 páginas, 7 figuras, 1 tabla.-- El pdf del artículo es la versión post-print. ; In this work we have studied the effect of caveolin-1 deficiency on the mechanisms that regulate free arachidonic acid (AA) availability. Results presented here demonstrate that macrophages from caveolin-1-deficient mice exhibit elevated fatty acid incorporation and remodeling and a constitutively increased CoA-independent transacylase activity. Mass spectrometry-based lipidomic analyses reveal stable alterations in the profile of AA distribution among phospholipids, manifested by reduced levels of AA in choline glycerophospholipids but elevated levels in ethanolamine glycerophospholipids and phosphatidylinositol. Furthermore, macrophages from caveolin-1 null mice show decreased AA mobilization and PGE 2 and LTB4 production upon cell stimulation. Collectively, these results provide insight into the role of caveolin-1 in AA homeostasis and suggest an important role for this protein in the eicosanoid biosynthetic response. ; This work was supported by the Spanish Ministry of Science and Innovation (Grants BFU2010-18826 and SAF2010-18831). A.M.A. was supported by a predoctoral fellowship from the Regional Government of Castile and León. ; Peer reviewed