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Abstract #0793

Magnetic susceptibility, R2* and iron evolve during reperfusion injury wound healing

Brianna F. Moon1, Srikant Kamesh Iyer2, Eileen Hwuang1, Nicholas J. Josselyn2, James J. Pilla2, Joseph H. Gorman III3, Robert C. Gorman3, Cory Tschabrunn4, Samuel J. Keeney3, Estibaliz Castillero5, Giovanni Ferrari5, Steffen Jockusch6, Haochang Shou7, Elizabeth M. Higbee-Dempsey8, Andrew Tsourkas1, Victor A. Ferrari4, Yuchi Han4, Harold I. Litt2, and Walter R. Witschey2
1Bioengineering, University of Pennsylvania, Philadelphia, PA, United States, 2Radiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States, 3Surgery, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States, 4Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States, 5Surgery, Columbia University Irving Medical Center, New York City, NY, United States, 6Chemistry, Columbia University, New York City, NY, United States, 7Biostatistics, Epidemiology and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States, 8Biochemistry and Molecular Biophysics Graduate Group, Perelman School of medicine, University of Pennsylvania, Philadelphia, PA, United States

There are multiple forms of iron including protein bound and labile iron found in reperfusion injury of acute myocardial infarction (MI). This study investigated iron accumulation, molecular form of iron, and cellular response to reperfusion injury with respect to the duration of wound-healing, in a large animal model. We demonstrate with magnetic susceptibility and R2* imaging biomarkers, there is a significant increase in infarct iron content in acute reperfusion injury that dissipates by 8-week post-MI and validate these findings with histology, iron concentration, and mRNA expression.

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