Supplementary Materials

Supplementary Materials for:

Interference with Akt Signaling Protects Against Myocardial Infarction and Death by Limiting the Consequences of Oxidative Stress

Bethany A. Kerr, Lining Ma, Xiaoxia Z. West, Liang Ding, Nikolay L. Malinin, Malory E. Weber, Mira Tischenko, Anna Goc, Payaningal R. Somanath, Marc S. Penn, Eugene A. Podrez, Tatiana V. Byzova*

*Corresponding author. E-mail: byzovat@ccf.org

This PDF file includes:

  • Fig. S1. Abundance of Akt signaling proteins in hearts, aortas, and livers.
  • Fig. S2. Akt1 deficiency results in diminished size.
  • Fig. S3. Akt1 deficiency is associated with decreased infarct size 4 weeks after coronary ligation.
  • Fig. S4. Akt1 deficiency on the ApoE−/− background leads to decreased aortic plaque formation in vivo and foam cell formation in vitro.
  • Fig. S5. Akt1 deficiency resulted in decreased hepatic hypertrophy and plasma triglyceride concentrations but no change in cholesterol concentrations.
  • Fig. S6. Akt1 deficiency does not affect plasma concentrations of catalase, superoxide dismutase, or nitrotyrosine and does not significantly alter CPP generation.
  • Fig. S7. CD36 protein abundance in macrophages.
  • Fig. S8. CD36 abundance is unchanged on ApoE−/− and ApoE−/−Akt1−/− macrophages.
  • Fig. S9. Blockade of CD36 diminished foam cell formation in wild-type and TKO macrophages.
  • Table S1. Akt1 deletion extends the fertile period of ApoE−/−SR-BI+/− mice.
  • Table S2. Genes encoding proatherosclerotic factors showing altered expression in isolated endothelial cells upon Akt1 deletion on the DKO background.
  • Reference (65)

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Citation: B. A. Kerr, L. Ma, X. Z. West, L. Ding, N. L. Malinin, M. E. Weber, M. Tischenko, A. Goc, P. R. Somanath, M. S. Penn, E. A. Podrez, T. V. Byzova, Interference with Akt Signaling Protects Against Myocardial Infarction and Death by Limiting the Consequences of Oxidative Stress. Sci. Signal. 6, ra67 (2013).

© 2013 American Association for the Advancement of Science