Coiled fiber scaffolds embedded with gold nanoparticles improve the performance of engineered cardiac tissues

Nanoscale ◽  
2014 ◽  
Vol 6 (16) ◽  
pp. 9410-9414 ◽  
Author(s):  
Sharon Fleischer ◽  
Michal Shevach ◽  
Ron Feiner ◽  
Tal Dvir
Keyword(s):  
Gold Nanoparticles ◽  
Cardiac Tissue ◽  
Cardiac Tissues ◽  
Fiber Scaffolds ◽  
Coiled Fiber

We report here on the fabrication of coiled fiber scaffolds incorporated with gold nanoparticles for improved cardiac tissue performance.

scholarly journals Modular assembly of thick multifunctional cardiac patches

2017 ◽  
Vol 114 (8) ◽  
pp. 1898-1903 ◽  
Author(s):  
Sharon Fleischer ◽  
Assaf Shapira ◽  
Ron Feiner ◽  
Tal Dvir
Keyword(s):  
Cardiac Tissue ◽  
Electrospun Fiber ◽  
Signal Propagation ◽  
Electrical Signal ◽  
Modular Assembly ◽  
Cardiac Tissues ◽  
Structure Morphology ◽  
Biomaterial Scaffolds ◽  
Fiber Scaffolds ◽  
And Function

In cardiac tissue engineering cells are seeded within porous biomaterial scaffolds to create functional cardiac patches. Here, we report on a bottom-up approach to assemble a modular tissue consisting of multiple layers with distinct structures and functions. Albumin electrospun fiber scaffolds were laser-patterned to create microgrooves for engineering aligned cardiac tissues exhibiting anisotropic electrical signal propagation. Microchannels were patterned within the scaffolds and seeded with endothelial cells to form closed lumens. Moreover, cage-like structures were patterned within the scaffolds and accommodated poly(lactic-co-glycolic acid) (PLGA) microparticulate systems that controlled the release of VEGF, which promotes vascularization, or dexamethasone, an anti-inflammatory agent. The structure, morphology, and function of each layer were characterized, and the tissue layers were grown separately in their optimal conditions. Before transplantation the tissue and microparticulate layers were integrated by an ECM-based biological glue to form thick 3D cardiac patches. Finally, the patches were transplanted in rats, and their vascularization was assessed. Because of the simple modularity of this approach, we believe that it could be used in the future to assemble other multicellular, thick, 3D, functional tissues.

scholarly journals Endurance Training Regulates Expression of Some Angiogenesis-Related Genes in Cardiac Tissue of Experimentally Induced Diabetic Rats

Biomolecules ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 498
Author(s):  
Mojdeh Khajehlandi ◽  
Lotfali Bolboli ◽  
Marefat Siahkuhian ◽  
Mohammad Rami ◽  
Mohammadreza Tabandeh ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endurance Training ◽  
Molecular Mechanisms ◽  
Cardiac Tissue ◽  
Critical Role ◽  
Diabetic Rats ◽  
Moderate Intensity ◽  
Pcr Analysis ◽  
Cardiac Tissues ◽  
The Impact

Exercise can ameliorate cardiovascular dysfunctions in the diabetes condition, but its precise molecular mechanisms have not been entirely understood. The aim of the present study was to determine the impact of endurance training on expression of angiogenesis-related genes in cardiac tissue of diabetic rats. Thirty adults male Wistar rats were randomly divided into three groups (N = 10) including diabetic training (DT), sedentary diabetes (SD), and sedentary healthy (SH), in which diabetes was induced by a single dose of streptozotocin (50 mg/kg). Endurance training (ET) with moderate-intensity was performed on a motorized treadmill for six weeks. Training duration and treadmill speed were increased during five weeks, but they were kept constant at the final week, and slope was zero at all stages. Real-time polymerase chain reaction (RT-PCR) analysis was used to measure the expression of myocyte enhancer factor-2C (MEF2C), histone deacetylase-4 (HDAC4) and Calmodulin-dependent protein kinase II (CaMKII) in cardiac tissues of the rats. Our results demonstrated that six weeks of ET increased gene expression of MEF2C significantly (p < 0.05), and caused a significant reduction in HDAC4 and CaMKII gene expression in the DT rats compared to the SD rats (p < 0.05). We concluded that moderate-intensity ET could play a critical role in ameliorating cardiovascular dysfunction in a diabetes condition by regulating the expression of some angiogenesis-related genes in cardiac tissues.

Pygo1 regulates pathological cardiac hypertrophy via a β-catenin-dependent mechanism

2021 ◽  
Author(s):  
Li Lin ◽  
Wei Xu ◽  
Yongqing Li ◽  
Ping Zhu ◽  
Wuzhou Yuan ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Cardiac Tissue ◽  
Heart Weight ◽  
Dependent Manner ◽  
Tissue Specific ◽  
Cardiac Tissues ◽  
Pathological Cardiac Hypertrophy ◽  
Interaction Factor ◽  
Myocardial Remodelling

Wnt/β-catenin signalling plays a key role in pathological cardiac remodelling in adults. The identification of a tissue-specific Wnt/β-catenin interaction factor may realise a tissue-specific clinical targeting strategy. Drosophila Pygo codes for the core interaction factor of Wnt/β-catenin. Two Pygo homologs, Pygo1 and Pygo2, have been identified in mammals. Different from the ubiquitous expression profile of Pygo2, Pygo1is enriched in cardiac tissue. However, the role of Pygo1 in mammalian cardiac disease remains unelucidated. Here, we found that Pygo1 was upregulated in human cardiac tissues with pathological hypertrophy. Cardiac-specific overexpression of Pygo1 in mice spontaneously led to cardiac hypertrophy accompanied by declined cardiac function, increased heart weight/body weight and heart weight/tibial length ratios and increased cell size. The canonical β-catenin/T-cell transcription factor 4 complex was abundant in Pygo1-overexpressingtransgenic(Pygo1-TG) cardiac tissue,and the downstream genes of Wnt signaling, i.e., Axin2, Ephb3, and C-myc, were upregulated. A tail vein injection of β-catenin inhibitor effectively rescued the phenotype of cardiac failure and pathological myocardial remodelling in Pygo1-TG mice. Furthermore, in vivo downregulated pygo1 during cardiac hypertrophic condition antagonized agonist-induced cardiac hypertrophy. Therefore, our study is the first to present in vivo evidence demonstrating that Pygo1 regulates pathological cardiac hypertrophy in a canonical Wnt/β-catenin-dependent manner, which may provide new clues for a tissue-specific clinical treatment targeting this pathway.

Methomyl induced effect on fortilin and S100A1 in serum and cardiac tissue: Potential biomarkers of toxicity

2018 ◽  
Vol 38 (3) ◽  
pp. 371-377
Author(s):  
SD Nusair ◽  
AN Joukhan ◽  
AH Bani Rashaid ◽  
AM Rababa’h
Keyword(s):  
Toxic Effect ◽  
Cardiac Tissue ◽  
Cardiac Fibroblasts ◽  
Study Group ◽  
Sprague Dawley ◽  
Cardiac Tissues ◽  
Sprague Dawley Rats ◽  
Cervical Dislocation ◽  
Potential Biomarkers

Methomyl toxicity has been reported as a cause of several accidental and suicidal fatalities. The study is evaluating the effect of lethal methomyl toxicity on fortilin and S100A1 in serum and cardiac tissues. Adult 96 female Sprague-Dawley rats were divided equally into a control (euthanized by cervical dislocation) and a study group (overdosed with methomyl). The levels of fortilin and S100A1 in serum were measured antemortem (to establish the basal levels in serum) and postmortem (to evaluate changes after methomyl exposure) using enzyme-linked immunoassay. S100A1 was immunostained in sections from cardiac tissues. Both proteins in the control were not significantly different ( p > 0.05) compared with the antemortem levels. On the contrast, both biomarkers levels in the intoxicated group were remarkably higher ( p < 0.001) than the control and the antemortem levels. Ventricular tissues from the intoxicated rats presented depleted S100A1 immunostain in cardiomyocytes localized mainly in the epicardium with deeply stained adjacent cardiac fibroblasts. The cardiomyocytes were damaged with a prominent loss of striations compared to normal cardiac tissues from the control. The present outcomes explain to a certain degree the potential toxic effect of methomyl poisoning on the cardiac tissue. Both proteins could be added to the currently available battery of markers for assessing methomyl toxicity.

Biophysical stimulation for in vitro engineering of functional cardiac tissues

2017 ◽  
Vol 131 (13) ◽  
pp. 1393-1404 ◽  
Author(s):  
Anastasia Korolj ◽  
Erika Yan Wang ◽  
Robert A. Civitarese ◽  
Milica Radisic
Keyword(s):  
Cardiac Tissue ◽  
Culture Media ◽  
Culture Conditions ◽  
Lineage Specification ◽  
Cardiac Tissues ◽  
Cardiac Lineage ◽  
And Function ◽  
Tissue Models

Engineering functional cardiac tissues remains an ongoing significant challenge due to the complexity of the native environment. However, our growing understanding of key parameters of the in vivo cardiac microenvironment and our ability to replicate those parameters in vitro are resulting in the development of increasingly sophisticated models of engineered cardiac tissues (ECT). This review examines some of the most relevant parameters that may be applied in culture leading to higher fidelity cardiac tissue models. These include the biochemical composition of culture media and cardiac lineage specification, co-culture conditions, electrical and mechanical stimulation, and the application of hydrogels, various biomaterials, and scaffolds. The review will also summarize some of the recent functional human tissue models that have been developed for in vivo and in vitro applications. Ultimately, the creation of sophisticated ECT that replicate native structure and function will be instrumental in advancing cell-based therapeutics and in providing advanced models for drug discovery and testing.

Abstract 30: In vitro Fabrication of Human Cardiac Tissues With Porcine Perfusable Blood Vessels

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Akitoshi Inui ◽  
Hidekazu Sekine ◽  
Kazunori Sano ◽  
Izumi Dobashi ◽  
Azumi Yoshida ◽  
...  
Keyword(s):  
Blood Vessels ◽  
Cardiac Tissue ◽  
Severe Heart Failure ◽  
Perfusion Culture ◽  
Cardiac Cell ◽  
Cell Sheets ◽  
Cardiac Tissues ◽  
Bioreactor System ◽  
Human Cardiac Tissue

The definitive treatment of severe heart failure is heart transplantation; however the number of heart transplantation procedures performed in Japan per year ranges from 30-40 due to donor shortage. Therefore, recently other treatments such as ventricular assist device or regenerative therapy by human cardiac tissue engineering have been developed and are considered as appropriate alternatives. We have developed an original technology, which was named cell-sheet based tissue engineering to fabricate functional three-dimensional tissue by layering cell sheets. The utilization of this technique allowed us to successfully engineer thick rat cardiac tissue with perfusable blood vessels in vitro. Here, we demonstrate a technique to engineer human cardiac tissue with perfusable blood vessels using cardiac cell sheets derived from human induced pluripotent stem cells, and porcine small intestine as a vascular bed for perfusion culture. The small intestine was harvested from with a branch of the superior mesenteric artery and vein and underwent mucosal resection after harvested tissue was cut open. To engineer cardiac tissue with perfusable blood vessels, cardiac cell sheets co-cultured with endothelial cells, were triple-layered and then was overlaid on the vascular bed in the bioreactor system. One day after perfusion culture, overlaid cardiac tissues pulsated spontaneously and were synchronized. The cardiac tissue construct was viable tissue without any observable necrosis. Furthermore we examined the possibility of transplantation of the in vitro engineered human cardiac tissue with the connectable host artery and vein. Engineered cardiac tissue was removed from the bioreactor system after 4-day perfusion, and transplanted to another pig heart. The branch of the superior mesenteric artery and vein of the graft were then reconnected to the host internal thoracic artery and vein. When the cardiac tissue reperfused, it began to beat spontaneously after a few minutes. We believe that this method is useful to fabricate functional cardiac tissue and may become an appropriate treatment for severe heart failure.

Electrophysiological derangements induced by lipid peroxidation in cardiac tissue

1987 ◽  
Vol 253 (5) ◽  
pp. H1089-H1097 ◽  
Author(s):  
H. Nakaya ◽  
N. Tohse ◽  
M. Kanno
Keyword(s):  
Lipid Peroxidation ◽  
Guinea Pig ◽  
Cardiac Tissue ◽  
Membrane Lipids ◽  
Cumene Hydroperoxide ◽  
Butylated Hydroxytoluene ◽  
Cardiac Tissues ◽  
Conduction Disturbances ◽  
Tert Butyl Hydroperoxide ◽  
Mda Content

Recently it has been postulated that oxygen-derived free radicals may be involved in reperfusion-induced arrhythmias. This study was undertaken to evaluate cellular electrophysiological alterations produced by peroxidation of membrane lipids in isolated cardiac tissues. In retrogradely perfused guinea pig hearts, perfusion of organic hydroperoxides, cumene hydroperoxide (CH), and tert-butyl hydroperoxide (TBH) caused conduction disturbances and arrhythmias, concomitantly with an increase in malondialdehyde (MDA) content of the myocardium. The hydroperoxides decreased the maximum diastolic potential, action potential amplitude, and maximum upstroke velocity of phase 0 in both canine Purkinje fibers and guinea pig papillary muscles. They also induced abnormal automaticity, such as depolarization-induced automaticity, delayed afterdepolarizations, and triggered activity. Mechanical abnormalities including increased resting tension and aftercontractions, presumably resulting from intracellular Ca2+ overload, were produced by the hydroperoxides. Pretreatment with butylated hydroxytoluene, an antioxidant, significantly inhibited the hydroperoxide-induced electrophysiological derangements and MDA accumulation in the myocardium. These results suggest that lipid peroxidation of membranes causes various electrophysiological and mechanical abnormalities and may play a role in the genesis of reperfusion-induced arrhythmias.

scholarly journals Virome Sequencing in Patients With Myocarditis

2020 ◽  
Vol 13 (7) ◽  
Author(s):  
Bettina Heidecker ◽  
Simon H. Williams ◽  
Komal Jain ◽  
Alexandra Oleynik ◽  
Dimitri Patriki ◽  
...  
Keyword(s):  
Peripheral Blood ◽  
Cardiac Tissue ◽  
Mononuclear Cells ◽  
Endogenous Retrovirus ◽  
Fulminant Myocarditis ◽  
Human Endogenous Retrovirus ◽  
Peripheral Blood Mononuclear ◽  
Tissue Samples ◽  
Cardiac Tissues ◽  
Barr Virus

Background: Polymerase chain reaction analyses of cardiac tissues have detected viral sequences in up to 67% of cases of myocarditis. However, viruses have not been implicated in giant cell myocarditis (GCM). Furthermore, efforts to detect viruses implicated in myocarditis have been unsuccessful in more accessible samples such as peripheral blood. Methods: We used Virome Capture Sequencing for Vertbrate Viruses (VirCapSeq-VERT), a method that simultaneously screens for all known vertebrate viruses, to investigate viruses in 33 patients with myocarditis. We investigated peripheral blood mononuclear cells (n=24), plasma (n=27), endomyocardial biopsies (n=2), and cardiac tissue samples from explanted hearts (n=13). Results: Nine patients (27%) had GCM and 4 patients (13%) had fulminant myocarditis. We found the following viruses in the blood of patients with myocarditis: Epstein Barr virus (n=11, 41%), human pegivirus (n=1, 4%), human endogenous retrovirus K (n=27, 100%), and anellovirus (n=15, 56%). All tissue samples from fulminant myocarditis (n=2) and GCM (n=13) contained human endogenous retrovirus K. Conclusions: No nucleic acids from viruses previously implicated in myocarditis or other human illnesses were detected in relevant amounts in cardiac tissue samples from GCM or in blood samples from other types of myocarditis. These findings do not exclude a role for viral infection in GCM but do suggest that if viruses are implicated, the mechanism is likely to be indirect rather than due to cytotoxic infection of myocardium.

1207Pulsed Field Ablation: Acute and Chronic Safety and Lesion Efficacy

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
A Verma ◽  
D Haines ◽  
N Kirchhof ◽  
B Onal ◽  
M Martien ◽  
...  
Keyword(s):  
Phrenic Nerve ◽  
Cardiac Tissue ◽  
Superior Vena ◽  
Vena Cava ◽  
Preclinical Study ◽  
Atrial Appendage ◽  
Right Atrial ◽  
Collateral Damage ◽  
Cardiac Tissues ◽  
Electrical Isolation

Abstract Introduction Thermal ablation methods are the cornerstone of treatment for atrial fibrillation. However, they pose a risk to extra-cardiac structures and may result in inadequate efficacy. Nonthermal, pulsed-field ablation (PFA) delivery to cardiac tissues may create durable, efficacious lesions while avoiding collateral damage. Purpose The purpose of this preclinical GLP study was to assess acute and chronic electrical isolation combined with a pathology assessment of chronic lesion extent in response to PFA delivery to cardiac tissue, and to document any collateral damage. Methods Six pigs were treated with biphasic, bipolar PFA doses through a circular multi-electrode catheter. PFA was delivered at four locations at specified voltages: superior vena cava (SVC at 700V), right atrial appendage (RAA at 1500V), left atrial appendage (LAA at 1200V), and right pulmonary vein (RPV at 1500V). Phrenic nerve pacing thresholds and electrical block at SVC, RPV, and RAA sites were investigated acutely, and electrical block at the SVC sites chronically. Pigs were survived for 4 weeks. After euthanasia, necropsies and histopathological assessments documented the findings at the lesion sites and collateral tissues. Results Post PFA, entrance block was achieved in all SVC, RPV, and RAA sites. Histopathology showed characteristic replacement fibrosis of the myocardium at all ablation sites. The PFA lesions in the SVC and RPV were all continuously circumferential and histopathology did not detect any remaining myofiber conduits across the post-ablation fibrosis (consistent with the electrical assessments). PFA of the appendages caused wide-ranging fibrosis in the RAA, and limited fibrosis in the LAA. Histologically, the atrial fibrosis was almost exclusively transmural in both, with the RAA lesions overall diagnosed as circumferentially complete in all but one case. The right phrenic nerve (RPN) pacing thresholds were unchanged from baseline to the end of the procedure and were all <1.0V. The examined juxtaposed RPN segments exposed to PFA at the SVC and RPV sites were normal. None of the ablated targets was associated with stenosis, aneurysms, luminal thrombus or collateral damage on the abluminal side. Continuous lesion sites Conclusions This limited preclinical study evaluated the acute and chronic safety and efficacy of PFA in multiple cardiac and vascular treatment sites. In this porcine model, PFA results in acute and chronic electrical isolation, confirmed by pathology data, for all of the RPV and SVC targets. Pathology findings of the RAA revealed the ability to achieve chronic transmural lesions in highly trabeculated cardiac tissue. No collateral damage was seen to the adjacent RPN. Acknowledgement/Funding Medtronic

scholarly journals The cardioprotective effects of the new crystal form of puerarin in isoproterenol-induced myocardial ischemia rats based on metabolomics

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yuzhi Zhou ◽  
Mengru Li ◽  
Jia Song ◽  
Yongqiang Shi ◽  
Xuemei Qin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Ischemia ◽  
Cardiac Tissue ◽  
Crystal Form ◽  
Cardiac Marker ◽  
Cardiac Tissues ◽  
Stress Indices ◽  
Cardioprotective Effects ◽  
Original Crystal ◽  
Better Than

Abstract Puerarin has shown unique pharmacological effects on myocardial ischemia (MI). Changing the crystal form is an effective approach to improve the cardioprotective effects of puerarin. However, the mechanisms of the new crystal form of puerarin are unclear. In this study, an electrocardiogram, echocardiography, cardiac marker enzymatic activity, oxidative stress indices, and myocardial histology analysis of cardiac tissues were performed to evaluate the cardioprotective effects of the new crystal form of puerarin. Moreover, serum and cardiac tissue metabolomics based on nuclear magnetic resonance (NMR) were used to investigate the potential mechanism of the new crystal form. The results indicated that the new crystal form of puerarin (30 mg/kg) could improve oxidative stress indices, and these improvements were similar to those of the original crystal form of puerarin (120 mg/kg). The new crystal form of puerarin (30 mg/kg) could effectively improve the activities of cardiac marker enzymes, and the improvement effects were better than those of the original crystal form (120 mg/kg). Moreover, metabolomics analysis showed that amino acid metabolism, oxidative stress and energy metabolism were disturbed after MI and could be improved by puerarin. These results demonstrated that the new crystal form of puerarin was effective in treating MI.

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