Figure 6.

The expression of eNOS by circulating bone marrow progenitor cells (BMPCs) contributes to myocardial recovery. (A) BMPCs from WT mice, BMPCs from eNOS-KO mice, or saline were intravenously injected into WT mice 24 hours after IR injury. Echocardiographic assessments of LV fractional shortening (FS) were performed before IR injury and 7–28 days afterward. (B–D) DiI-labeled WT BMPCs, DiI-labeled eNOS-KO BMPCs, or saline was intravenously injected into WT mice 24 hours after IR injury and treatment with subcutaneous injections of AMD3100 or saline; mice were sacrificed 2 days later (i.e., 3 days after IR injury). ^§Bonferroni-adjusted P<0.05 versus saline; ^#P<0.05 and ^##P<0.01 versus before injection. (B) Incorporation of the injected cells was evaluated by quantifying the number of DiI-positive cells in the AAR; scale bar=100 um. (C) Sections from the AAR were TUNEL-stained (green), stained with fluorescent anti-alpha-sarcomeric actin antibodies (red), and counterstained with DAPI (blue); scale bar=100 um. Apoptosis was quantified as the number of TUNEL+ cells. (D) Infarct size and AAR were assessed via in-vivo microsphere perfusion and TTC staining; viable tissue appears deep red and the infarcted region is colorless. The ratio of the area of the infarct to the AAR was presented as a percentage. *P<0.05 and **P<0.01; ^#P<0.05 and ^##P<0.01 versus the same intravenous injection (i.e., saline, WT BMPCs, or eNOS-KO BMPCs) in animals treated with subcutaneous injections of saline; NS, not significant. Panel A: n=4–5 per treatment group at each time point; Panel B: n=3–5 per group; Panel C: n=3–7 per group; Panel D: n=4–7 per group.