The reduction of hemodynamic loading assists self-regeneration of the injured heart by increasing cell proliferation, inhibiting cell apoptosis, and inducing.

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The reduction of hemodynamic loading assists self-regeneration of the injured heart by increasing cell proliferation, inhibiting cell apoptosis, and inducing stem-cell recruitment Ryo Suzuki, MD, Tao-Sheng Li, MD, PhD, Akihito Mikamo, MD, PhD, Masaya Takahashi, MD, Mako Ohshima, MS, Masayuki Kubo, PhD, Hiroshi Ito, MD, PhD, Kimikazu Hamano, MD, PhD The Journal of Thoracic and Cardiovascular Surgery Volume 133, Issue 4, Pages 1051-1058 (April 2007) DOI: 10.1016/j.jtcvs.2006.12.026 Copyright © 2007 The American Association for Thoracic Surgery Terms and Conditions

Figure 1 Morphologic and histologic findings of self-repair of the infarcted heart under loading and unloading conditions. A, The anterior wall of the infarcted left ventricle was replaced completely by thin scar tissue (arrow) in the loading heart (left), whereas the left ventricle anterior wall appeared to be thick with less scar tissue (arrowhead) in the unloading heart (right) 28 days after infarction. B, The ventricular weight decreased gradually in the unloading group but was increased 28 days after infarction in the loading group. Closed bar, loading group; open bar, unloading group; *P < .05, **P < .01. C, Hematoxylin–eosin staining showed that the infarcted myocardium was replaced completely by fibrotic tissue in the loading heart 28 days after infarction, whereas layers of cardiomyocytes (arrow) were observed distinctly in the endocardium of the infarcted left ventricle in the unloading heart. D, Quantitative analysis showed that the wall thickness of the infarcted left ventricle was significantly less in the loading group than in the unloading group 28 days after infarction. E, Azan staining showed a larger fibrotic area (blue) in the loading heart than in the unloading heart. F, Quantitative analysis showed that the area of infarction was significantly greater in the loading group than in the unloading group 28 days after infarction. The Journal of Thoracic and Cardiovascular Surgery 2007 133, 1051-1058DOI: (10.1016/j.jtcvs.2006.12.026) Copyright © 2007 The American Association for Thoracic Surgery Terms and Conditions

Figure 2 The proliferation of cells in the injured heart. A, Representative photograph of the proliferating cells. The proliferation of cells was identified by immunostaining with the nuclear antigen of Ki-67 (red, left), and nuclei were stained by DAPI (blue, middle). Scale bars: 20 μm. B, Quantitative counting of Ki-67-positive cells with a myocyte-specific morphologic structure revealed significantly fewer proliferating cells in the loading group than in the unloading group 7 days after infarction. The Journal of Thoracic and Cardiovascular Surgery 2007 133, 1051-1058DOI: (10.1016/j.jtcvs.2006.12.026) Copyright © 2007 The American Association for Thoracic Surgery Terms and Conditions

Figure 3 The apoptosis of cells in the injured heart. A, Representative photograph of the apoptotic cells. TUNEL-positive cells were labeled by green (left), and nuclei were stained by DAPI (blue, middle). Scale bars: 20 μm. B, Quantitative counting of TUNEL-positive cells with a myocyte-specific morphologic structure revealed significantly more apoptotic cells in the loading group than in the unloading group 3 and 7 days after infarction. The Journal of Thoracic and Cardiovascular Surgery 2007 133, 1051-1058DOI: (10.1016/j.jtcvs.2006.12.026) Copyright © 2007 The American Association for Thoracic Surgery Terms and Conditions

Figure 4 The c-kit-positive stem cells in the injured heart. A, Representative photograph of the c-kit-positive stem cells in the infarcted heart. The c-kit-positive cells were stained by red (left), and nuclei were stained by DAPI (blue, middle). Scale bars: 20 μm. B, Quantitative analysis revealed significantly more c-kit-positive cells in the loading group than in the unloading group 7 days after infarction. The Journal of Thoracic and Cardiovascular Surgery 2007 133, 1051-1058DOI: (10.1016/j.jtcvs.2006.12.026) Copyright © 2007 The American Association for Thoracic Surgery Terms and Conditions

Figure 5 Sca-1-positive stem cells in the injured heart. A, Representative photograph of the Sca-1-positive cells in the infarcted heart. The Sca-1-positive cells were stained by red (left), and nuclei were stained by DAPI (blue, middle). Scales bars: 20 μm. B, Quantitative analysis revealed significantly more Sca-1-positive cells in the loading group than in the unloading group 7 days after infarction. The Journal of Thoracic and Cardiovascular Surgery 2007 133, 1051-1058DOI: (10.1016/j.jtcvs.2006.12.026) Copyright © 2007 The American Association for Thoracic Surgery Terms and Conditions

Figure 6 The expression of SDF-1α in the heart 3 and 7 days after infarction. Immunostaining analysis revealed that the expression of SDF-1α was relatively weak in the loading heart (A); however, intensive expression of SDF-1α was observed in the unloading heart, especially in the border area of the infarcted myocardium. The Journal of Thoracic and Cardiovascular Surgery 2007 133, 1051-1058DOI: (10.1016/j.jtcvs.2006.12.026) Copyright © 2007 The American Association for Thoracic Surgery Terms and Conditions