Arterial spin labeling CMR quantifies increased perfusion in hearts of mice treated with cardioprotective, AAV9-mediated
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BioMed Central
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Poster presentation
Arterial spin labeling CMR quantifies increased perfusion in hearts of mice treated with cardioprotective, AAV9-mediated EcSOD gene therapy prior to myocardial infarction Brent A French*, Konkal-Matt R Prasad, Moriel H Vandsburger, Ronald J Beyers, Yaqin Xu, Robert L Janiczek, Craig H Meyer and Frederick H Epstein Address: University of Virginia, Charlottesville, VA, USA * Corresponding author
from 13th Annual SCMR Scientific Sessions Phoenix, AZ, USA. 21-24 January 2010 Published: 21 January 2010 Journal of Cardiovascular Magnetic Resonance 2010, 12(Suppl 1):P212
doi:10.1186/1532-429X-12-S1-P212
Abstracts of the 13th Annual SCMR Scientific Sessions - 2010
Meeting abstracts - A single PDF containing all abstracts in this Supplement is available here. http://www.biomedcentral.com/content/files/pdf/1532-429X-11-S1-infoThis abstract is available from: http://jcmr-online.com/content/12/S1/P212 © 2010 French et al; licensee BioMed Central Ltd.
Introduction Experimental myocardial infarction (MI), direct gene transfer with adeno-associated viral (AAV) vectors and CMR in mice are powerful tools for studying the roles of individual genes in MI and post-MI left ventricular (LV) remodeling. Arterial spin labeling (ASL) enables the quantification of myocardial perfusion (MP) by CMR, but is sensitive to variable heart rates and irregular respiration, prohibiting accurate measurement early after MI. We developed a cardio-respiratory gated (CRG) ASL method that is insensitive to these factors to measure MP in mice.
moter (AcTnTEcSOD or AcTnTeGFP), and were injected IV into 4-5 week-old C57Bl/6 mice (3 × 1011 vp/mouse). Four weeks after injection, MI was induced by a 30 min coronary occlusion. Infarct size and area at risk (A@R) were measured 24 h later by TTC and Phthalo blue staining, respectively. Capillary density was measured 4 wks post injection in remote myocardium immunostained for CD31.
Results
The objective of this study was to test the hypotheses that AAV9-mediated overexpression of extracellular superoxide dismutase (EcSOD) from the cardiac Troponin-T (cTnT) promoter would increase capillary density and protect the heart against myocardial infarction (MI). Furthermore, we tested the hypothesis that an improved method of ASL could quantitate the elevation in MP resulting from increased capillary density.
MP as measured by CRG-ASL increased by 30% from 4.3 + 0.5 before to 5.6 + 0.3 ml/g-min at 4 wks post AcTnTEcSOD injection (P < 0.05), then dropped to 2.4 + 0.6 ml/gmin in the infarct zone 24 h post-MI. A single IV injection of AcTnTEcSOD provided uniform EcSOD overexpression throughout the myocardium (Panel A). Infarct size (as % A@R, Panel B) was reduced by 45% in EcSOD mice (33.9 + 6.3, mean + SEM, n = 4) compared to eGFP mice (61.3 + 3.8, n = 4, P < 0.05). Capillary density was 23.6% higher in EcSOD mice (5446 + 368/mm2) compared to eGFP mice (4405 + 271/mm2, P < 0.05), Figure 1.
Methods
Conclusion
CRG-ASL was developed on a 7 T MR system and em
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