Abstract
In this work we have studied the effect of caveolin-1 deficiency on the mechanisms that regulate free arachidonic acid (AA) availability. The 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 prostaglandin E(2) and LTB(4) 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.
Highlights
We have studied the effect of caveolin-1 deficiency on the mechanisms that regulate free arachidonic acid availability
To assess a possible role for caveolin-1 in arachidonic acid (AA) incorporation into the various lipid classes of mouse peritoneal macrophages, cells from the caveolin-1 null mouse strain described by Lisanti and co-workers [20] and from their littermate wild type controls were exposed to various concentrations of [3H]AA, and the incorporation into phospholipid versus TAG was measured
Caveolin-1 is expressed in all cells and tissues, it is especially abundant in adipocytes and endothelial cells [14]
Summary
We have studied the effect of caveolin-1 deficiency on the mechanisms that regulate free arachidonic acid availability. Results: Macrophages from caveolin-1-deficient mice exhibit elevated fatty acid incorporation and remodeling and a constitutively increased CoA-independent transacylase activity. Conclusion: Macrophages from caveolin-1 null mice show decreased arachidonate mobilization and eicosanoid production upon cell stimulation. The 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. Macrophages from caveolin-1 null mice show decreased AA mobilization and prostaglandin E2 and LTB4 production upon cell stimulation. 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
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