scholarly journals Self-assembling peptide hydrogel enables instant epicardial coating of the heart with mesenchymal stromal cells for the treatment of heart failure

Biomaterials ◽  
2018 ◽  
Vol 154 ◽  
pp. 12-23 ◽  
Author(s):  
Yuki Ichihara ◽  
Masahiro Kaneko ◽  
Kenichi Yamahara ◽  
Marinos Koulouroudias ◽  
Nobuhiko Sato ◽  
...  
2021 ◽  
Vol 1 (1) ◽  
pp. 2-7
Author(s):  
Carla Longo de Freitas ◽  
Priscilla Yuri Okochi Alves da silva ◽  
Maria do Carmo Pinho Franco ◽  
Danilo Candido De Almeida

The new pandemic of SARS-CoV-2 Betacoronavirus, has spread worldwide, and infected millions of individuals causing the disease denominated of COVID-19. Further on flu symptoms, due to the high tropism of virus, has most been observed in the COVID-19 pathophysiology: acute heart failure, thromboembolism events, acute renal failure, neurological and liver damage, and multiple organ failure, with special attention to endothelial disfunction. Hence, elucidate whether virus target the endothelium is a crucial step to understand COVID-19 pathogenesis. However, the permissiveness of blood vessels during SARS-CoV-2 infection remains unclear, but regardless endothelial infection, the vascular disfunction may occurred in response to molecular inflammatory signaling triggered by immune cells that attempt to limit infection. Thus, alternative therapies using mesenchymal stromal cells (MSCs) can change this scenario and help critically ill patients. In this reflection, we attempt to discuss COVID-19 pathophysiology with impact in endothelial function and explore the applicability of MSC-based therapies as alternative treatment.  


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.


2021 ◽  
Vol 10 (3) ◽  
Author(s):  
Amarachukwu Okpala ◽  
Leya Joykutty

Heart disease is one of the leading causes of morbidity and mortality worldwide. Two of these diseases are heart failure and myocardial infarction. In America alone, there are about 6.2 million people with heart failure, and every 40 seconds, a patient with a heart attack is recorded. Myocardial infarction, known as a heart attack, occurs after the blocking or occlusion of a coronary artery, disabling the delivery of oxygenated blood to regions of the heart. Heart failure, usually occurring after ischemic diseases like myocardial infarction, is where the heart loses the ability to pump a sufficient blood supply to meet the body’s needs. The major ways of treating heart failure and myocardial infarction today are either too expensive or hard to come by, so a new sort of treatment is direly needed. Cellular cardiomyoplasty, a form of cell therapy, is being looked into as a new way to treat these two and other cardiomyopathies. Additionally, though there have been a few cells that have shown a possibility of use for cardiomyoplasty, this review focuses on mesenchymal stem cells, specifically called mesenchymal stromal cells. The purpose of this review is to look into what cellular cardiomyoplasty is, how it may be used in the future, and how mesenchymal stromal cells have shown potential to be used for it.


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