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. Author manuscript; available in PMC: 2013 Jul 9.
Published in final edited form as: Am J Physiol Heart Circ Physiol. 2012 Aug 17;303(8):H967–H978. doi: 10.1152/ajpheart.00040.2012

Fig. 3.

Fig. 3

Upregulation and translocation of cryAB and PcryAB to the mitochondria under oxidative stress conditions. A: immunoblots of cryAB and PcryAB along with actin standards in WT mouse adult CM controls or CMs exposed to 100 μM H2O2 for 1 h. B: quantification of cryAB and PcryAB levels in adult mouse CMs after exposure to 100 μM H2O2 relative to control levels (*P < 0.05). C: immunoblots of cytosolic and organellar subcellular fractions for cryAB and PcryAB in cultured neonatal CMs under control conditions and after exposure to 60 μM H2O2. The distribution of VDAC, a mitochondrial marker, and GAPDH, a cytosolic marker, was assessed to monitor the purity of the fractions. D: quantification of the mitochondrial and cytosolic distribution of cryAB and PcryAB in cultured neonatal CMs after exposure to 60 μM H2O2 relative to control conditions (#P < 0.05). The band intensities of cryAB organellar levels are expressed in arbitrary units (AU). Values are reported as means ± SE; n = 3. *P < 0.05, mitochondria vs. control cytosol conditions; **P < 0.05, mitochondria vs. stress cytosol conditions.