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. Author manuscript; available in PMC: 2013 Mar 1.
Published in final edited form as: Mitochondrion. 2011 Sep 10;12(2):180–189. doi: 10.1016/j.mito.2011.08.011

Figure 1. STAT3 expression in heart mitochondria affects mitochondrial function.

Figure 1

(A) Cardiac-specific deletion of STAT3 results in a 50% decrease in complex I activity (Wegrzyn et al., 2009), whereas mitochondria-targeted over expression of STAT3 (MLS-STAT3E) leads to a modest 20% reduction in complex I activity (Szczepanek et al., 2011). Results are means ± SEM, n=4 for both groups. (B) Over expression of mitochondria-targeted, transcriptionally inactive STAT3 (MLS-STAT3E) decreases ROS production and blocks cytochrome c release during ischemia (Szczepanek et al., 2011). Results are means ± SEM, n=4 for both groups. Y axis depicts the ischemia-induced increase in net release of H2O2 from mitochondria respiring with glutamate+malate as complex I substrate, expressed as percent increase compared to time control (mitochondria from non-ischemic hearts). X axis depicts cytochrome c release and is shown as a percent decrease in signal compared to cytochrome c in time control samples.