Figure 6.
CXCR4 activation in neutrophils protects fromI/Rinjury. (a) AAR (left graph) of the myocardium in vehicle- and ATI-treated mice infarcted at ZT5 and infarct sizes (right graph) after correction for AAR from the same animals subjected to MI and followed by 24 h of reperfusion; n = 5 mice per group. Representative images of infarcted hearts from vehicle- and ATI-treated mice at ZT5 after 24 h of reperfusion. Dotted black lines highlight areas of dead myocardium. Analysis was performed 24 h after infarction (the following day at ZT5). (b) AAR (left graph) of the myocardium in vehicle- and agonist-treated WT and CXCR4ΔN mice infarcted at ZT5 and infarct sizes (right graph) after correction for AAR from the same animals subjected to MI and followed by 1 h of reperfusion; n = 4–5 mice per group. Representative images of infarcted hearts from vehicle- and agonist-treated CXCR4ΔN mice at ZT5. Dotted black lines highlight areas of dead myocardium. Analysis was performed 1 h and 45 min after infarction. (c) Experimental scheme to analyze cardiac function by echocardiography at different times after CXCR4 agonist treatment and permanent MI induced at ZT5. Analysis of cardiac function was performed at ZT5 at day 0 (basal, before infarction) and at day 3 and day 28 after infarction. (d) Segmental wall motion of the myocardium. Colors reflect the different severities of segmental wall movement: noninfarction, normokinesis, hypokinesis, akinesis, and aneurysm. (e) Selected cardiac parameters measured by echocardiography in vehicle and ATI2341-treated mice at different times. Left atrium area (LA Area), left atrium volume (LA Volume), left atrium ejection fraction (LA EF), left atrium fraction shortening (LA FS), severity score, and number of myocardial affected segments are shown. Some parameters were measured at diastole (d); n = 5–8 mice per group. Data in a–e are from single experiments. Data are shown as the mean ± SEM.; ***P < 0.001; ns, not significant, as determined by unpaired t test analysis (a) and two-way ANOVA (b and e).

CXCR4 activation in neutrophils protects from I/R injury. (a) AAR (left graph) of the myocardium in vehicle- and ATI-treated mice infarcted at ZT5 and infarct sizes (right graph) after correction for AAR from the same animals subjected to MI and followed by 24 h of reperfusion; n = 5 mice per group. Representative images of infarcted hearts from vehicle- and ATI-treated mice at ZT5 after 24 h of reperfusion. Dotted black lines highlight areas of dead myocardium. Analysis was performed 24 h after infarction (the following day at ZT5). (b) AAR (left graph) of the myocardium in vehicle- and agonist-treated WT and CXCR4ΔN mice infarcted at ZT5 and infarct sizes (right graph) after correction for AAR from the same animals subjected to MI and followed by 1 h of reperfusion; n = 4–5 mice per group. Representative images of infarcted hearts from vehicle- and agonist-treated CXCR4ΔN mice at ZT5. Dotted black lines highlight areas of dead myocardium. Analysis was performed 1 h and 45 min after infarction. (c) Experimental scheme to analyze cardiac function by echocardiography at different times after CXCR4 agonist treatment and permanent MI induced at ZT5. Analysis of cardiac function was performed at ZT5 at day 0 (basal, before infarction) and at day 3 and day 28 after infarction. (d) Segmental wall motion of the myocardium. Colors reflect the different severities of segmental wall movement: noninfarction, normokinesis, hypokinesis, akinesis, and aneurysm. (e) Selected cardiac parameters measured by echocardiography in vehicle and ATI2341-treated mice at different times. Left atrium area (LA Area), left atrium volume (LA Volume), left atrium ejection fraction (LA EF), left atrium fraction shortening (LA FS), severity score, and number of myocardial affected segments are shown. Some parameters were measured at diastole (d); n = 5–8 mice per group. Data in a–e are from single experiments. Data are shown as the mean ± SEM.; ***P < 0.001; ns, not significant, as determined by unpaired t test analysis (a) and two-way ANOVA (b and e).

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