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J Biol Chem, Vol. 274, Issue 33, 23085-23093, August 13, 1999

Interleukin 1 Induces Type II-secreted Phospholipase A₂ Gene in Vascular Smooth Muscle Cells by a Nuclear Factor B and Peroxisome Proliferator-activated Receptor-mediated Process

From the Unité Propre de Recherche de l'Université Pierre et Marie Curie, Associée au CNRS, ESA7079, 7 quai St. Bernard, 75252 Paris, Cedex 5, France

Type II-secreted phospholipase A₂ (type II-sPLA₂) is expressed in smooth muscle cells during atherosclerosis or in response to interleukin-1. The present study shows that the induction of type II-sPLA₂ gene by interleukin-1 requires activation of the NFB pathway and cytosolic PLA₂/PPAR pathway, which are both necessary to achieve the transcriptional process. Interleukin-1 induced type II-sPLA₂ gene dose- and time-dependently and increased the binding of NFB to a specific site of type II-sPLA₂ promoter. This effect was abolished by proteinase inhibitors that block the proteasome machinery and NFB nuclear translocation. Type II-sPLA₂ induction was also obtained by free arachidonic acid and was blocked by either AACOCF₃, a specific cytosolic-PLA₂ inhibitor, PD98059, a mitogen-activated protein kinase kinase inhibitor which prevents cytosolic PLA₂ activation, or nordihydroguaiaretic acid, a lipoxygenase inhibitor, but not by the cyclooxygenase inhibitor indomethacin, suggesting a role for a lipoxygenase product. Type II-sPLA₂ induction was obtained after treatment of the cells by 15-deoxy-^12,14-dehydroprostaglandin J₂, carbaprostacyclin, and 9-hydroxyoctadecadienoic acid, which are ligands of peroxisome proliferator-activated receptor (PPAR) , whereas PPAR ligands were ineffective. Interleukin-1 as well as PPAR-ligands stimulated the activity of a reporter gene containing PPAR-binding sites in its promoter. Binding of both NFB and PPAR to their promoter is required to stimulate the transcriptional process since inhibitors of each class block interleukin-1-induced type II-sPLA₂ gene activation. We therefore suggest that NFB and PPAR cooperate at the enhanceosome-coactivator level to turn on transcription of the proinflammatory type II-sPLA₂ gene.

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