Cardiac-specific catalase overexpression rescues anthrax lethal toxin-induced cardiac contractile dysfunction: role of oxidative stress and autophagy
1 Center for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, WY 82071, USA
2 Cancer Research Institute of Scott & White Memorial Hospital, Temple, TX 76502, USA
BMC Medicine 2012, 10:134 doi:10.1186/1741-7015-10-134Published: 7 November 2012
Additional file 1:
Figure S1: Effect of catalase overexpression on LeTx exposure-induced changes in intracellular Ca2+ regulatory proteins. A: Representative gel blots depicting expression of SERCA2a, Na+-Ca2+ exchanger (NCX), phospholamban (PLB), phosphorylated PLB and GAPDH (used as loading control); B: SERCA2a; C: NCX; and D: phosphorylated-PLB (p-PLB)-to-PLB ratio. Mean ± SEM, n = 6 mice per group, *P <0.05 vs. WT group. Figure S2: Effect of autophagy induction or inhibition on lethal toxin induced cardiac contractile dysfunction. A-B: Isolated cardiomyocytes from WT and CAT mice were incubated with lethal toxin (100 ng/ml) for 3 h in presence or absence of the autophagy inhibitor 3-methyladenine (3-MA, 10 mM) or autophagy inducer rapamycin (5 μM) respectively. A: Resting cell length; B: time-to-peak shortening (TPS). Mean ± SEM, n = 60 to 75 cells from three mice per group, *P <0.05 vs. WT group, # P <0.05 vs. WT-LeTx group.
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