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. Author manuscript; available in PMC: 2015 Oct 4.

Published in final edited form as: Cardiology. 2014 Oct 4;129(3):163–173. doi: 10.1159/000363646

Fig. 2 — IPC increases Akt localization to the plasma membrane through PTEN signaling pathway. A-B: Distribution of Caveolin (Cav)-3 and Akt in subcellular fractions. Isolated hearts from WT or PKO mice were treated with no ischemia (CON), I-10/R-5 (IPC), IPC+LY (LY20094, 10 μM), or CON+AI (Akt Inhibitor, 20 μM). Subcellular fractionations were performed with sucrose gradient centrifugation. Equal volumes of cell lysates were loaded onto SDS PAGE gels. Protein expression of caveolin (Cav)-3 was measured. Representative blots from at least three independent experiments. C: Akt protein levels in Cav-3-enriched fractions. Equal amounts of protein from Cav-3-enriched fractions were loaded. N = 4/group, *: p<0.01 vs. CON/WT or IPC/LY; #: p<0.01 vs. CON/PKO.

Fig. 2 — IPC increases Akt localization to the plasma membrane through PTEN signaling pathway. A-B: Distribution of Caveolin (Cav)-3 and Akt in subcellular fractions. Isolated hearts from WT or PKO mice were treated with no ischemia (CON), I-10/R-5 (IPC), IPC+LY (LY20094, 10 μM), or CON+AI (Akt Inhibitor, 20 μM). Subcellular fractionations were performed with sucrose gradient centrifugation. Equal volumes of cell lysates were loaded onto SDS PAGE gels. Protein expression of caveolin (Cav)-3 was measured. Representative blots from at least three independent experiments. C: Akt protein levels in Cav-3-enriched fractions. Equal amounts of protein from Cav-3-enriched fractions were loaded. N = 4/group, *: p<0.01 vs. CON/WT or IPC/LY; #: p<0.01 vs. CON/PKO.