Objective-To determine the role of prostacyclin (PGI 2 ) in protecting endothelial cells (ECs) from apoptosis and elucidate the protective mechanism. Methods and Results-To evaluate the effect of PGI 2 on EC survival, we treated ECs with Ad-COX1/PGIS (Ad-COPI), which augmented selectively PGI 2 production or carbaprostacyclin (cPGI 2 ) followed by H 2 O 2 for 4 hours. Ad-COPI inhibited annexin V-positive cells and blocked caspase 3 activation. cPGI 2 inhibited apoptosis in a concentrationdependent manner. L-165041 had a similar effect, suggesting the involvement of peroxisome proliferator-activated receptor-␦ (PPAR␦). ECs expressed functional PPAR␦. PPAR␦ overexpression enhanced whereas PPAR␦ knockdown by small interfering RNA abrogated the antiapoptotic action of cPGI 2 and L-165041. Our results show for the first time that PGI 2 stimulated 14-

To determine the role of 14-

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