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. Author manuscript; available in PMC: 2010 May 19.
Published in final edited form as: Circulation. 2009 May 4;119(19):2587–2596. doi: 10.1161/CIRCULATIONAHA.108.827691

Figure 2.

Figure 2

Representative blots showing higher phosphorylation of (A) IGF-1R and (B) Akt in PCSca-1+ as compared to non-PCSca-1+. Treatment of the cells with PI-3K inhibitor (LY294002; 40μM) prior to preconditioning abolished pAkt under normoxia and after 8-h OGD. Total Akt remained unchanged. (C) LDH release assay showed that cell death was attenuated in PCSca-1+ as compared to non-PCSca-1+ under 8-h OGD. Pretreatment of cells with LY294002 abolished the cytoprotective effects of preconditioning under OGD. (D1) Downstream of pAkt, caspase-3 cleavage (active form) was significantly prevented in PCSca-1+ which otherwise was increased in non-PCSca-1+ under 8-h OGD. Pre-treatment of cells with LY294002 increased caspase-3 cleavage. (D2) Cells treated with caspase-3 inhibitor (Z-DEVD-FMK; 20μM) showed lower cell death as compared to the cells treated with DMSO (vehicle of caspase inhibitor).