scholarly journals Preconditioning of skeletal myoblast-based engineered tissue constructs enables functional coupling to myocardium in vivo

2015 ◽  
Vol 149 (1) ◽  
pp. 348-356 ◽  
Author(s):  
Philipp Treskes ◽  
Klaus Neef ◽  
Sureshkumar Perumal Srinivasan ◽  
Marcel Halbach ◽  
Christof Stamm ◽  
...  
2013 ◽  
Vol 61 (S 01) ◽  
Author(s):  
K Neef ◽  
P Treskes ◽  
S Kumar ◽  
M Khalil ◽  
OJ Liakopoulos ◽  
...  

2020 ◽  
Vol 15 (1) ◽  
pp. 1177-1192
Author(s):  
Soumen Jana ◽  
Amir Lerman

Aim: We aimed to develop a leaflet-shaped trilayered tissue construct mimicking the morphology of native heart valve leaflets. Materials & methods: Electrospinning and in vivo tissue engineering methods were employed. Results: We developed leaflet-shaped microfibrous scaffolds, each with circumferentially, randomly and radially oriented three layers mimicking the trilayered, oriented structure of native leaflets. After 3 months in vivo tissue engineering with the scaffolds, the generated leaflet-shaped tissue constructs had a trilayered structure mimicking the orientations of native heart valve leaflets. Presence of collagen, glycosaminoglycans and elastin seen in native leaflets was observed in the engineered tissue constructs. Conclusion: Trilayered, oriented fibrous scaffolds brought the orientations of the infiltrated cells and their produced extracellular matrix proteins into the constructs.


Author(s):  
Jacob Bennedsen ◽  
Karen Chang Yan

Engineered tissue constructs are assembled through combining scaffolds, cells and biologically active molecules for restoring, maintaining, or improving damaged tissues or whole organs. Cells in engineered tissue constructs often experience mechanical forces during the fabrication process, maturation process, and under in vivo conditions. These mechanical forces/stimuli induce cellular responses and affect cell viability, proliferation, and differentiation. While it is critical to understand the mechanical milieu of cells in tissue constructs, it is also extremely challenging due to the time and length scale span. Multiscale modeling approaches have been emerged to provide linkage among different length scale. One of the approaches is continuum based multiscale modeling to link organ, tissue and cellular levels. A representative volume element (RVE) with periodic or random microstructure serves as a vehicle to connect different length scales. This study focuses on effects of RVE selection, microstructure, and boundary conditions on the mechanical environment at cellular level. In particular, cell embedded alginate tissue constructs were studied. Hyperelastic models were used for modeling alginate and cells. Multi-cellular FE models were generated. The results of the average properties and the stress/strain experienced by cells were compared under different conditions.


2014 ◽  
Vol 62 (S 01) ◽  
Author(s):  
K. Neef ◽  
A.-C. Deppe ◽  
S. Srinivasan ◽  
P. Treskes ◽  
C. Stamm ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Irza Sukmana

The guidance of endothelial cell organization into a capillary network has been a long-standing challenge in tissue engineering. Some research efforts have been made to develop methods to promote capillary networks inside engineered tissue constructs. Capillary and vascular networks that would mimic blood microvessel function can be used to subsequently facilitate oxygen and nutrient transfer as well as waste removal. Vascularization of engineering tissue construct is one of the most favorable strategies to overpass nutrient and oxygen supply limitation, which is often the major hurdle in developing thick and complex tissue and artificial organ. This paper addresses recent advances and future challenges in developing three-dimensional culture systems to promote tissue construct vascularization allowing mimicking blood microvessel development and function encounteredin vivo. Bioreactors systems that have been used to create fully vascularized functional tissue constructs will also be outlined.


Biology ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 539
Author(s):  
Khaled M. A. Abdel-Raouf ◽  
Rachid Rezgui ◽  
Cesare Stefanini ◽  
Jeremy C. M. Teo ◽  
Nicolas Christoforou

The development of robust skeletal muscle models has been challenging due to the partial recapitulation of human physiology and architecture. Reliable and innovative 3D skeletal muscle models recently described offer an alternative that more accurately captures the in vivo environment but require an abundant cell source. Direct reprogramming or transdifferentiation has been considered as an alternative. Recent reports have provided evidence for significant improvements in the efficiency of derivation of human skeletal myotubes from human fibroblasts. Herein we aimed at improving the transdifferentiation process of human fibroblasts (tHFs), in addition to the differentiation of murine skeletal myoblasts (C2C12), and the differentiation of primary human skeletal myoblasts (HSkM). Differentiating or transdifferentiating cells were exposed to single or combinations of biological ligands, including Follistatin, GDF8, FGF2, GDF11, GDF15, hGH, TMSB4X, BMP4, BMP7, IL6, and TNF-α. These were selected for their critical roles in myogenesis and regeneration. C2C12 and tHFs displayed significant differentiation deficits when exposed to FGF2, BMP4, BMP7, and TNF-α, while proliferation was significantly enhanced by FGF2. When exposed to combinations of ligands, we observed consistent deficit differentiation when TNF-α was included. Finally, our direct reprogramming technique allowed for the assembly of elongated, cross-striated, and aligned tHFs within tissue-engineered 3D skeletal muscle constructs. In conclusion, we describe an efficient system to transdifferentiate human fibroblasts into myogenic cells and a platform for the generation of tissue-engineered constructs. Future directions will involve the evaluation of the functional characteristics of these engineered tissues.


2014 ◽  
Vol 83 (2) ◽  
pp. 759-768 ◽  
Author(s):  
Sabrina Torre ◽  
Sebastien P. Faucher ◽  
Nassima Fodil ◽  
Silayuv E. Bongfen ◽  
Joanne Berghout ◽  
...  

We identify anN-ethyl-N-nitrosourea (ENU)-induced I23N mutation in the THEMIS protein that causes protection against experimental cerebral malaria (ECM) caused by infection withPlasmodium bergheiANKA.ThemisI23Nhomozygous mice show reduced CD4+and CD8+T lymphocyte numbers. ECM resistance inP. bergheiANKA-infectedThemisI23Nmice is associated with decreased cerebral cellular infiltration, retention of blood-brain barrier integrity, and reduced proinflammatory cytokine production. THEMISI23Nprotein expression is absent from mutant mice, concurrent with the decreased THEMISI23Nstability observedin vitro. Biochemical studiesin vitroand functional complementationin vivoinThemisI23N/+:Lck−/+doubly heterozygous mice demonstrate that functional coupling of THEMIS to LCK tyrosine kinase is required for ECM pathogenesis. Damping of proinflammatory responses inThemisI23Nmice causes susceptibility to pulmonary tuberculosis. Thus, THEMIS is required for the development and ultimately the function of proinflammatory T cells.ThemisI23Nmice can be used to study the newly discovered association ofTHEMIS(6p22.33) with inflammatory bowel disease and multiple sclerosis.


2010 ◽  
Vol 2010 (4) ◽  
pp. pdb.prot5416-pdb.prot5416 ◽  
Author(s):  
R. A. Poche ◽  
J. E. Saik ◽  
J. L. West ◽  
M. E. Dickinson

2021 ◽  
Author(s):  
Jung-Hwan Choi ◽  
Lauren Bayer Horowitz ◽  
Niels Ringstad

At chemical synapses, neurotransmitters are packaged into synaptic vesicles that release their contents in response to depolarization. Despite its central role in synaptic function, regulation of the machinery that loads vesicles with neurotransmitters remains poorly understood. We find that synaptic glutamate signaling in a C. elegans chemosensory circuit is regulated by antagonistic interactions between the canonical vesicular glutamate transporter EAT-4/VGLUT and another vesicular transporter, VST-1. Loss of VST-1 strongly potentiates glutamate release from chemosensory BAG neurons and disrupts chemotaxis behavior. Analysis of the circuitry downstream of BAG neurons shows that excess glutamate release disrupts behavior by inappropriately recruiting RIA interneurons to the BAG-associated chemotaxis circuit. Our data indicate that in vivo the strength of glutamatergic synapses is controlled by regulation of neurotransmitter packaging into synaptic vesicles via functional coupling of VGLUT and VST-1.


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