Figure 3
SDF-1 gene transfer improves cardiac function through increased angiogenesis. At 8 weeks after plasmid injection, animals were killed and the hearts processed for immunohistochemistry. Slides were stained for von Willebrand factor and ventricular myosin for blood vessels and myocytes, respectively, in the infarct zone after injection with SDF-1 plasmid in the pCMV- and pCMVe-treated animals. (a) Vessel density was significantly increased in the SDF-1-treated animals when compared with control animals. pCMVe-SDF1, 21±1.82 vessels mm−2; pCMV-SDF1, 17±1.48 vessels mm−2 and saline controls 6±0.73 vessels mm−2. *P<0.001, n=7 in all groups. (b) Echocardiographic assessment following plasmid injection. Pre-injection (1 month after infarct), all rats had a fractional shortening (FS) <30%. At 4 weeks after injection, the control group (n=10) decreased in FS by 35.97±11.08 CMV-driven plasmids showed a statistically significant improvement of 4.32±26.10% (pCMV-SDF1) (n=9) and 24.97±28.87% (pCMVe-SDF1) (n=10), respectively, **P<0.05. The cardiac-specific promoter plasmid (pMHC-SDF1) (n=9) did not improve function compared with control. (c) Comparative analysis between the percentage of FS at 4 and 8 weeks. The improvement in cardiac function, as observed at 4 weeks was sustained at 8 weeks after injections.
