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Adipose tissue secretes proinflammatory mediators which promote systemic and adipose tissue inflammation seen in obesity. Group IIA (GIIA)-secreted phospholipase A 2 (sPLA 2 ) enzymes are found to be elevated in plasma and adipose tissue from obese patients and are active during inflammation, generating proinflammatory mediators, including prostaglandin E 2 (PGE 2 ). PGE 2 exerts anti-lipolytic actions and increases triacylglycerol levels in adipose tissue. However, the inflammatory actions of GIIA sPLA 2 s in adipose tissue cells and mechanisms leading to increased PGE 2 levels in these cells are unclear. This study investigates the ability of a representative GIIA sPLA 2 , MT-III, to activate proinflammatory responses in preadipocytes, focusing on the biosynthesis of prostaglandins, adipocytokines and mechanisms involved in these effects. Our results showed that MT-III induced biosynthesis of PGE 2 , PGI 2 , MCP-1, IL-6 and gene expression of leptin and adiponectin in preadipocytes. The MT-III-induced PGE 2 biosynthesis was dependent on cytosolic PLA 2 (cPLA 2 )-α, cyclooxygenases (COX)-1 and COX-2 pathways and regulated by a positive loop via the EP 4 receptor. Moreover, MT-III upregulated COX-2 and microsomal prostaglandin synthase (mPGES)-1 protein expression. MCP-1 biosynthesis induced by MT-III was dependent on the EP4 receptor, while IL-6 biosynthesis was dependent on EP3 receptor engagement by PGE 2 . These data highlight preadipocytes as targets for GIIA sPLA 2 s and provide insight into the roles played by this group of sPLA 2 s in obesity.

A Representative GIIA Phospholipase A2 Activates Preadipocytes to Produce Inflammatory Mediators Implicated in Obesity Development