Effect of MFN2 deficiency on mitochondrial Bax translocation, and outer membrane injury.

<p>(<b>A</b>) Immunoblot of Bax (<i>upper panel</i>) in mitochondrial membrane fractions of MFN2^f/f proximal tubule epithelial cells exposed to no virus (<i>NT</i>), empty virus (<i>CTL</i>) or Cre adenovirus (<i>MFN2-</i>) at baseline and 30 min post ATP-depletion; F₁F₀ ATPase serves as loading control (<i>lower panel</i>). (<b>B</b>) Immunoblot analysis of cytochrome c (<i>upper panel</i>) and Apoptosis Inducing Factor (AIF) (<i>middle panel</i>) in cytosolic fractions harvested from non-viral transduced cells (<i>NT</i>) or cells transduced with either empty virus (<i>CTL</i>) or Cre adenovirus (<i>MFN2-</i>) at baseline and 30 min after ATP depletion. ß-actin loading control (<i>lower panel</i>). (<b>C</b>) Densitometric analysis of mitochondrial Bax accumulation as well as the leakage of cytochrome c and AIF in renal tubule epithelial cells after ATP depletion; data represent the mean and SE of 4 separate experiments; <i>P</i><0.05.