scholarly journals Local activation of cardiac stem cells for post-myocardial infarction cardiac repair

2012 ◽  
Vol 16 (11) ◽  
pp. 2549-2563 ◽  
Author(s):  
Zhuzhi Wen ◽  
Zun Mai ◽  
Haifeng Zhang ◽  
Yangxin Chen ◽  
Dengfeng Geng ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Stem Cells ◽  
Cardiac Repair ◽  
Post Myocardial Infarction ◽  
Cardiac Stem Cells ◽  
Local Activation

Abstract 19337: Transcoronary Delivery of Allogeneic Cardiac Stem Cells Reduces Ventricular Arrhythmia Inducibility in a Post Myocardial Infarction Swine Model

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Gerard Loughlin ◽  
Pablo M Ruiz Hernandez ◽  
Pablo Avila ◽  
Veronica Crisostomo ◽  
Ricardo Sanz ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Stem Cells ◽  
Ventricular Arrhythmia ◽  
Electrophysiological Study ◽  
Post Myocardial Infarction ◽  
Control Group ◽  
P Value ◽  
Swine Model ◽  
Cardiac Stem Cells ◽  
Electroanatomic Mapping System

Introduction: Post myocardial infarction (MI) patients are at risk of scar related ventricular tachycardia (VT). Hypothesis: Stem cell therapy reduces post-MI scar size, potentially leading to a reduction in the risk of ventricular arrhythmias (VA). Methods: A post-MI scar model of VT was created by transient occlusion of the mid left anterior descending artery in 56 swine. Five weeks after infarct creation 29 subjects were treated with allogeneic cardiac stem cells (CSC): 10 underwent transcoronary delivery of CSC, 9 direct transepicardial delivery (via a minithoracotomy) and 10 underwent a combined transcoronary and VT substrate guided (late potentials) direct transendocardial CSC delivery procedure using an electroanatomic mapping system. Of the remainder, 8 subjects underwent a “sham” transepicardial procedure and 19 served as controls. Seventeen weeks after infarct creation an electrophysiological study was performed in each subject to assess for ventricular arrhythmia inducibility. VA inducibility was compared in each group vs. the control group. Results: Of the 19 control subjects, 17 were inducible (89,5 %). As presented in the figure, CSC delivery with a combined transcoronary/transendocardial approach was associated with a significant reduction in VT inducibility rates compared to controls (20 % vs. 89,5 %; p value 0,001). Subjects treated with transcoronary CSC also experienced significantly lower VA inducibility rates (40 % vs. 89,5 %; p value 0,009). There were no differences in VA inducibility compared with controls in patients in the “sham” (62,5 % vs 89,5 %; p value 0,136) or the transepicardial group (66,7 % vs 89,5 %; p value 0,290). Conclusions: Combined transcoronary and VT substrate-guided transendocardial CSC delivery is associated with a significant reduction in VA inducibility in a post-MI swine model. Future human studies should evaluate the effects of allogeneic CSC therapy on ventricular arrhythmia burden in post-MI patients.

scholarly journals INCREASED POTENCY OF CARDIAC STEM CELLS COMPARED TO BONE MARROW MESENCHYMAL STEM CELLS IN CARDIAC REPAIR

2011 ◽  
Vol 57 (14) ◽  
pp. E1014
Author(s):  
Behzad Nasehi Oskouei ◽  
Guillaume Lamirault ◽  
Chacko Joseph ◽  
Stephanie Landa ◽  
Marc Dauer ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Cardiac Repair ◽  
Cardiac Stem Cells ◽  
Marrow Mesenchymal Stem Cells

scholarly journals Heart Repair Using Nanogel-Encapsulated Human Cardiac Stem Cells in Mice and Pigs with Myocardial Infarction

ACS Nano ◽  
2017 ◽  
Vol 11 (10) ◽  
pp. 9738-9749 ◽  
Author(s):  
Junnan Tang ◽  
Xiaolin Cui ◽  
Thomas G. Caranasos ◽  
M. Taylor Hensley ◽  
Adam C. Vandergriff ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Stem Cells ◽  
Cardiac Stem Cells ◽  
Heart Repair

Abstract 13: Plasminogen Is Required for Hematopoietic Stem Cell-Mediated Cardiac Repair After Myocardial Infarction

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Yanqing Gong ◽  
Jane Hoover-Plow ◽  
Ying Li
Keyword(s):  
Myocardial Infarction ◽  
Stem Cells ◽  
Bone Marrow ◽  
Stem Cell ◽  
Tissue Repair ◽  
Critical Role ◽  
Cardiac Repair ◽  
Internal Diameter ◽  
Hematopoietic Stem

Ischemic heart disease, including myocardial infarction (MI), is the primary cause of death throughout the US. Granulocyte colony-stimulating factor (G-CSF) is used to mobilize hematopoietic progenitor and stem cells (HPSC) to improve cardiac recovery after MI. However, poor-mobilization to G-CSF is observed in 25% of patients and 10-20% of healthy donors. Therefore, a better understanding of the underlying mechanisms regulating G-CSF-induced cardiac repair may offer novel approaches for strengthening stem cell-mediated therapeutics. Our previous studies have identified an essential role of Plg in HPSC mobilization from bone marrow (BM) in response to G-CSF. Here, we investigate the role of Plg in G-CSF-stimulated cardiac repair after MI. Our data show that G-CSF significantly improves cardiac tissue repair including increasing neovascularization in the infarct area, and improving ejection fraction and LV internal diameter by echocardiogram in wild-type mice. No improvement in tissue repair and heart function by G-CSF is observed in Plg -/- mice, indicating that Plg is required for G-CSF-regulated cardiac repair after MI. To investigate whether Plg regulates HPSC recruitment to ischemia area, bone marrow transplantion (BMT) with EGFP-expressing BM cells was performed to visualize BM-derived stem cells in infarcted tissue. Our data show that G-CSF dramatically increases recruitment of GFP+ cells (by 16 fold) in WT mice but not in Plg -/- mice, suggesting that Plg is essential for HPSC recruitment from BM to the lesion sites after MI. In further studies, we investigated the role of Plg in the regulation of SDF-1/CXCR-4 axis, a major regulator for HPSC recruitment. Our results show that G-CSF significantly increases CXCR-4 expression in infarcted area in WT mice. While G-CSF-induced CXCR-4 expression is markedly decreased (80%) in Plg -/- mice, suggesting Plg may regulate CXCR-4 expression during HSPC recruitment to injured heart. Interestingly, Plg does not affect SDF-1 expression in response to G-CSF treatment. Taken together, our findings have identified a critical role of Plg in HSPC recruitment to the lesion site and subsequent tissue repair after MI. Thus, targeting Plg may offer a new therapeutic strategy to improve G-CSF-mediated cardiac repair after MI.

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