scholarly journals Functional Recovery after Intramyocardial Injection of Adipose-Derived Stromal Cells Assessed by Cardiac Magnetic Resonance Imaging

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Janusz Konstanty-Kalandyk ◽  
Jerzy Sadowski ◽  
Anna Kędziora ◽  
Małgorzata Urbańczyk-Zawadzka ◽  
Jakub Baran ◽  
...  

Aims. A major clinical concern is the continuous increase in the number of patients diagnosed with advanced coronary artery disease, ischemic heart failure, and refractory angina, and one of the most promising treatment options for these conditions is stem cell-based therapy. The aim of this study was to assess the functional improvement following intramyocardial injection of adipose-derived stromal cells, using cardiac magnetic resonance. Methods and Results. Thirteen patients with ischemic heart failure, reduced left ventricular ejection fraction, refractory angina, and who have been disqualified from any form of direct revascularization were enrolled in the study with transthoracic autologous adipose-derived stromal cell implantation. All patients underwent cardiac magnetic resonance prior to the procedure and after 12 months of follow-up. A significant increase in stroke volume ( 83.1 ± 8.5   mL vs 93.8 ± 13.8   mL , p = 0.025 ) and stroke volume index ( 43.3 ± 7.6   mL / m 2 vs 48.7 ± 9.1   mL / m 2 , p = 0.019 ), a statistical trend toward an increase in left ventricle ejection fraction ( 36.7 ± 13.2 vs 39.7 ± 14.9 , p = 0.052 ), and cardiac output improvement ( 5.0 ± 0.7 vs 5.5 ± 0.9 , p = 0.073 ) was observed in the patient postprocedure. Enhanced relative regional thickening was noted in the segments with adipose-derived stromal cell implantation. Conclusions. Intramyocardial adipose-derived stromal cell implantation is a promising therapeutic option for selected, symptomatic patients with ischemic heart failure, who have preserved myocardial viability despite being unsuitable for direct revascularization.

2012 ◽  
Vol 18 (3) ◽  
pp. MT19-MT25 ◽  
Author(s):  
Katarzyna Gruszczyńska ◽  
Łukasz J. Krzych ◽  
Krzysztof S. Gołba ◽  
Jolanta Biernat ◽  
Tomasz Roleder ◽  
...  

2020 ◽  
Vol 126 (7) ◽  
pp. 857-874 ◽  
Author(s):  
Wenjun Yan ◽  
Chen Lin ◽  
Yongzhen Guo ◽  
Youhu Chen ◽  
Yunhui Du ◽  
...  

Rationale: Mesenchymal stromal cell–based therapy is promising against ischemic heart failure. However, its efficacy is limited due to low cell retention and poor paracrine function. A transmembrane protein capable of enhancing cell-cell adhesion, N-cadherin garnered attention in the field of stem cell biology only recently. Objective: The current study investigates whether and how N-cadherin may regulate mesenchymal stromal cells retention and cardioprotective capability against ischemic heart failure. Methods and Results: Adult mice–derived adipose tissue–derived mesenchymal stromal cells (ADSC) were transfected with adenovirus harboring N-cadherin, T-cadherin, or control adenovirus. CM-DiI-labeled ADSC were intramyocardially injected into the infarct border zone at 3 sites immediately after myocardial infarction (MI) or myocardial ischemia/reperfusion. ADSC retention/survival, cardiomyocyte apoptosis/proliferation, capillary density, cardiac fibrosis, and cardiac function were determined. Discovery-driven/cause-effect analysis was used to determine the molecular mechanisms. Compared with ADSC transfected with adenovirus-control, N-cadherin overexpression (but not T-cadherin) markedly increased engrafted ADSC survival/retention up to 7 days post-MI. Histological analysis revealed that ADSC transfected with adenovirus-N-cadherin significantly preserved capillary density and increased cardiomyocyte proliferation and moderately reduced cardiomyocyte apoptosis 3 days post-MI. More importantly, ADSC transfected with adenovirus-N-cadherin (but not ADSC transfected with adenovirus-T-cadherin) significantly increased left ventricular ejection fraction and reduced fibrosis in both MI and myocardial ischemia/reperfusion mice. In vitro experiments demonstrated that N-cadherin overexpression promoted ADSC-cardiomyocyte adhesion and ADSC migration, enhancing their capability to increase angiogenesis and cardiomyocyte proliferation. MMP (matrix metallopeptidases)-10/13 and HGF (hepatocyte growth factor) upregulation is responsible for N-cadherin’s effect upon ADSC migration and paracrine angiogenesis. N-cadherin overexpression promotes cardiomyocyte proliferation by HGF release. Mechanistically, N-cadherin overexpression significantly increased N-cadherin/β-catenin complex formation and active β-catenin levels in the nucleus. β-catenin knockdown abolished N-cadherin overexpression–induced MMP-10, MMP-13, and HGF expression and blocked the cellular actions and cardioprotective effects of ADSC overexpressing N-cadherin. Conclusions: We demonstrate for the first time that N-cadherin overexpression enhances mesenchymal stromal cells–protective effects against ischemic heart failure via β-catenin-mediated MMP-10/MMP-13/HGF expression and production, promoting ADSC/cardiomyocyte adhesion and ADSC retention.


2017 ◽  
Vol 6 (11) ◽  
pp. 1963-1971 ◽  
Author(s):  
Jens Kastrup ◽  
Mandana Haack-Sørensen ◽  
Morten Juhl ◽  
Rebekka Harary Søndergaard ◽  
Bjarke Follin ◽  
...  

2011 ◽  
Vol 44 (4) ◽  
pp. 293-299 ◽  
Author(s):  
Seok-Min Kang ◽  
Jong-Chul Park ◽  
Min-Jeong Shin ◽  
Hyeran Lee ◽  
Jaewon Oh ◽  
...  

2003 ◽  
Vol 42 (12) ◽  
pp. 2063-2069 ◽  
Author(s):  
Pieter C Smits ◽  
Robert-Jan M van Geuns ◽  
Don Poldermans ◽  
Manolis Bountioukos ◽  
Emile E.M Onderwater ◽  
...  

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