Modulation of Lipid Body Biogenesis in Epithelial Cells

Abstract

Lipid Bodies are cytoplasmic inclusions mainly formed by triglycerides and cholesterol esters, being also intracellular deposits of arachidonic acid (AA), which can be metabolized for eicosanoids generation. PGE2 is a major AA metabolite produced by epithelial cells and can modulate restoration of epithelium homeostasis after injury. We studied lipid body biogenesis and their role in AA metabolic pathway in epithelial cells. A rat cell line derived from normal intestinal epithelium, IEC‐6, was used. IEC‐6 in sub‐confluent cultures presented 15–20 lipid bodies/cell after staining with by OsO4. Lipid bodies were virtually absent in IEC‐6 upon reaching confluency or after FBS withdraw. Stimulation of confluent IEC‐6 with IL‐1β, PAF, or PMA was unable to induce lipid bodies. In contrast, AA dose‐dependently induced lipid body formation and proliferation foci in confluent cultures independently of its metabolism to PGE2. AA induction of lipid bodies was dependent on signaling through p38, PKC, and PI3K, but not ERK 1/2 or JNK. Lipid body biogenesis facilitates AA release after ionophore activation without modifying cPLA2α expression. Our results suggest a strong relationship between lipid body biogenesis and epithelial cell proliferation, and indicate that these organelles are induced in a stimulus‐specific manner and facilitate AA mobilization in epithelial cells.Financial support: CNPq, FAPERJ, CAPES