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Peroxisome proliferator-activated receptor-gammaprotects cerebral endothelial cells against hypoxic injury

Jui-Sheng Wu1,2, Yu-Chang Chen1, Hsin-Da Tsai1, Teng-Nan Lin1
1Neuroscience Division, Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, R.O.C.
2Graduate Institute of Life Sciences, NationalDefenseMedicalCenter; 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. Immuno-fluorescence cytochemistry studies further revealed that PGJ2 protects CECs by attenuating OGD-induced 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,

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