Chronic phospholamban inhibition prevents progressive cardiac dysfunction and pathological remodeling after infarction in rats
J. Clin. Invest. Yoshitaka Iwanaga, et al. 113:727 doi:10.1172/JCI18716 [Go to this article.]

Figure 5
S16EPLN transgene expression and suppression of histological signs of cardiac remodeling after S16EPLN gene transfer. (A) RT-PCR confirmation of transgene expression in noninfarcted myocardium isolated from S16EPLN-treated hearts at 6 months after gene transfer. Extracted RNA was treated with DNase before RT-PCR. Primers were designed within 5′ noncoding and 3′ noncoding sequences in rAAV-S16EPLN vector, flanking the S16EPLN cDNA coding sequence. (B–D) Representative images of Masson’s trichrome staining (× 200): no-MI (B), MI-saline (C), and MI-S16EPLN animals (D). (E and F) Myocyte diameters (E) and fibrosis areas (F) were quantitatively analyzed as described in Methods. Studies occurred at 6 months after gene transfer. Data represent mean ± SE. *P < 0.05 between groups (n = 5 per group).