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ToF‐SIMS analysis of myocardial infarcted tissue
Author(s) -
Park JiWon,
Cha MinJi,
Kyong Shon Hyun,
Kim SeHwa,
Lee Tae Geol,
Moon Dae Won,
Hwang KiChul
Publication year - 2011
Publication title -
surface and interface analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.52
H-Index - 90
eISSN - 1096-9918
pISSN - 0142-2421
DOI - 10.1002/sia.3628
Subject(s) - mesenchymal stem cell , myocardial infarction , phosphocholine , chemistry , cell , fatty acid , border zone , biochemistry , adipose tissue , cell membrane , membrane , pathology , medicine , phospholipid , phosphatidylcholine
Heart tissues from a normal rat, myocardial infarcted rat, and mesenchymal stem cell (MSC)‐treated rat after myocardial infarction (MI) were studied using ToF‐SIMS, with the assistance of principal component analysis (PCA). To our knowledge, this is the first such published study. In PCA results obtained from both positive and negative ion spectra of normal (control), MI, and MSC‐treated MI tissues, the normal and MSC‐treated tissues could be clearly distinguished from the MI tissue in terms of chemical composition. For the MI tissue, fatty acid signals from inside the cell and phosphocholine signals from the cell membrane decreased while glucose signals increased. In the MSC‐treated MI tissue, the signal levels of phosphocholine and fatty acids returned to those for normal tissue. Our observations for myocardium tissues are consistent with previous biological studies, which show that the loss of reversibility of cell injury associated with MI could cause degradation to the cell membrane, and that MI could slow fatty acid uptake and oxidation and increase glucose uptake and utilization for ATP synthesis in myocardium. This is, of course, because fatty acids need oxygen for β‐oxidation. We anticipate that this label‐free ToF‐SIMS method partnered with PCA will be helpful to the investigation of myocardial disease and MSC therapy since it is based on chemical information at the tissue level. Copyright © 2010 John Wiley & Sons, Ltd.