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1 Cardiovascular Division, University of Minnesota, Minneapolis, MN, USA
2 Department of Medicine, University of Buffalo, Buffalo, NY, USA
* To whom correspondence should be addressed. E-mail: zhang047{at}umn.edu.
In an established swine model of severe left ventricular hypertrophy (LVH), the bioenergetic and functional consequences of transplanting autologous mesenchymal stem cells over-expressing vascular endothelial growth factor (VEGF-MSCs) into the LV were evaluated; transplantation was accomplished by infusion of VEGF-MSCs into the interventricular cardiac vein. Specifically, the hypertrophic response to aortic banding was compared in 7 pigs treated with 30 million VEGF-MSCs, 8 pigs treated with 30 million MSCs without VEGF modification and 19 untreated LVH pigs. 8 pigs without banding or cell transplantation (N) were also studied. Four weeks post-banding, LV wall thickening (MRI), myocardial blood flow (MBF), high-energy phosphate levels (31P-MRS) and hemodynamic measurements were obtained under basal conditions and during a catecholamine induced high cardiac workstate (HCW). Although 9 of 19 untreated banded pigs developed clinical evidence of biventricular failure, no MSCs treated animal developed heart failure. MSCs engraftment was present in both cell transplant groups and both baseline and HCW MBF values were significantly increased in hearts receiving VEGFMSCs as compared to other groups (p<0.05). During HCW, cardiac inotropic reserve (defined as the percent increase of rate-pressure product at HCW relative to baseline) was normal in the VEGF-MSCs group and significantly decreased in all other banded groups. Additionally, during HCW the myocardial energetic state (reflected by the phosphocreatine-to-ATP ratio; PCr/ATP) of VEGF-MSCs treated hearts remained stable whereas in all other groups PCr/ATP decreased significantly from baseline values (p<0.05, each). Myocardial von Willebrand factor and VEGF mRNA expressions and myocardial capillary density were significantly increased in VEGFMSCs treated hearts (p<0.05). Hence, in the pressure overloaded LV, transplantation of VEGF MSCs prevents LV decompensation, induces neovascularization, attenuates hypertrophy, and improves MBF, myocardial bioenergetic characteristics and contractile performance.
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