1 ABSTRACT AND POSTER INSTRUCTIONS PLEASE TYPE YOUR ABSTRACT IN THE BOX BELOW Please prepare your abstract in WORD file, limited to 350 words (Arial 10) in text. (Example below) Underline the presenting author’s name. Email Registration Form and Abstract to: antgopal@nus.edu.sg Poster size: A1 SIZE UPRIGHT POSTER (23X33 Inches) Example of Abstract Peroxisome proliferator-activated receptor-gamma protects cerebral endothelial cells against hypoxic Injury Jui-Sheng Wu1,2, Yu-Chang Chen1, Hsin-Da Tsai1, Teng-Nan Lin1 1Neuroscience 2Graduate Division, Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, R.O.C. Institute of Life Sciences, National Defense Medical Center; Taipei, Taiwan Peroxisome proliferator-activated receptor gamma (PPAR-r) is a nuclear membrane-associated transcription factor that governs various genes, including lipid biosynthesis, glucose metabolism and inflammatory. Several lines of evidence suggest that PPAR-r agonists protect brain against ischemia/reperfusion injury; however, the exact mechanisms are not clear. Previously, we have shown that intra-ventricular infusion of 15d-PGJ2 (a physiological agonist for PPAR-r) reduced cerebral infarct and this protective effect were abolished by inhibitor of PPAR-r. Interestingly, up-to-date all the beneficial effects of PPAR-r against cerebral ischemia were demonstrated in neuron, astrocyte and microglial, but not in endothelial cells. To investigate the possible role of PPAR-r in ischemia induced cerebral endothelial cells (CECs) death, murine CECs culture were exposed to oxygen-glucose deprivation (OGD) with or without the presence of PPAR-r agonist (15d-PGJ2 or rosiglitazone) and antagonist (GW9662). Western blot analysis was used to study the temporal profiles of proteins. Apoptotic cell death was analyzed by flow cytometry. PPAR-r activity was analyzed by luciferase reported assay. Plasmid and siRNA transfection were used to over-express or silence PPAR-r. We have demonstrated the existence of PPAR-r in CECs by RT-PCR; nevertheless, level of PPAR-r is much less in CECs than in neural cells. Phase-contrast photomicrographs showed a sharp decrease in the number of CECs after OGD; cell loss was rescued by 15d-PGJ2 and rosiglitazone; this beneficial effect was blunted by BADGE. Immunofluorescence cytochemistry studies further revealed that PGJ2 protects CECs by attenuating OGDinduced DNA condensation and caspase 3 activation. PGJ2 also attenuated the breakdown of PARP-1. Results of flow cytometry showed that 15d-PGJ2 inhibited OGD-induced endothelial apoptosis, which was abrogated by BADGE. Moreover, over expression of PPAR-r also attenuated OGD-induced death of CECs, and this protective effect was further enhanced in the presence of PGJ2. In summary, our results suggest that PPAR-r protects endothelial cells against ischemic-induced apoptosis. Keywords: 15d-PGJ2, PPAR-r, endothelium, rosiglitazone