Fig. 2.

Spry1 cardiomyocyte knockdown protects from ischemia–reperfusion injury in vivo. Wild-type (WT), Spry1^fl/fl and Spry1 cardiomyocyte knockout (cKO) mice were subjected to 30 min of cardiac ischemia and 24 h of reperfusion, and subjected to analysis of infarct size, serum troponin I levels and analysis of cardiac function by echocardiography. a Analysis for area at risk (AAR) and infarct size relative to AAR derived from triphenyltetrazolium chloride (TTC) stainings. N = 9–13 per group. b Analysis for troponin I levels from serum samples. N = 9–13 per group. c Spry1^fl/fl and Spry1 cKO mice were subjected to 30 min of ischemia and 6 h of reperfusion, and subjected to analysis for serum troponin I levels and apoptosis by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). Shown are also representative images of TUNEL labeling of sections from hearts of Spry1^fl/fl and Spry1 cKO mice. Scale bar 40 µm. N = 11–13 per group. *P < 0.05 versus WT mice and ^#P < 0.05, ^##P < 0.01 versus Spry1^fl/fl mice