Use of an in vitro model in tissue engineering to study wound repair and differentiation of blastema tissue from rabbit pinna

2015 ◽  
Vol 51 (7) ◽  
pp. 680-689 ◽  
Author(s):  
Mohammad Reza Hashemzadeh ◽  
Nasser Mahdavi-Shahri ◽  
Ahmad Reza Bahrami ◽  
Masoumeh Kheirabadi ◽  
Fatemeh Naseri ◽  
...  
2003 ◽  
Vol 9 (2) ◽  
pp. 233-241 ◽  
Author(s):  
Dara Chafik ◽  
David Bear ◽  
Phong Bui ◽  
Arush Patel ◽  
Neil F. Jones ◽  
...  

Polymers ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1478 ◽  
Author(s):  
Samuel R. Moxon ◽  
Miguel J.S. Ferreira ◽  
Patricia dos Santos ◽  
Bogdan Popa ◽  
Antonio Gloria ◽  
...  

Degeneration of articular cartilage (AC) is a common healthcare issue that can result in significantly impaired function and mobility for affected patients. The avascular nature of the tissue strongly burdens its regenerative capacity contributing to the development of more serious conditions such as osteoarthritis. Recent advances in bioprinting have prompted the development of alternative tissue engineering therapies for the generation of AC. Particular interest has been dedicated to scaffold-based strategies where 3D substrates are used to guide cellular function and tissue ingrowth. Despite its extensive use in bioprinting, the application of polycaprolactone (PCL) in AC is, however, restricted by properties that inhibit pro-chondrogenic cell phenotypes. This study proposes the use of a new bioprintable poly(ester urea) (PEU) material as an alternative to PCL for the generation of an in vitro model of early chondrogenesis. The polymer was successfully printed into 3D constructs displaying adequate substrate stiffness and increased hydrophilicity compared to PCL. Human chondrocytes cultured on the scaffolds exhibited higher cell viability and improved chondrogenic phenotype with upregulation of genes associated with type II collagen and aggrecan synthesis. Bioprinted PEU scaffolds could, therefore, provide a potential platform for the fabrication of bespoke, pro-chondrogenic tissue engineering constructs.


Author(s):  
Christine Obbink-Huizer ◽  
Cees W. J. Oomens ◽  
Sandra Loerakker ◽  
Jasper Foolen ◽  
Carlijn V. C. Bouten ◽  
...  

In many tissue engineering applications it is essential to understand how cells orient under the influence of their mechanical environment. In vitro engineered models are used to investigate the orientation of F-actin stress fibers inside cells. One such in vitro model [1] consists of a mixture of cells, collagen and matrigel, that is constrained by an array of silicone posts (Figure 1). We have recently developed a computational model to describe the orientation of stress fibers in response to their mechanical environment [2]. In the present study, this computational model is extended to 3D and used to simulate cell behavior in the mentioned in vitro model. This improves our understanding of how stress fibers orient in response to the mechanical environment and aids in optimizing the use of the in vitro model.


2016 ◽  
Vol 24 ◽  
pp. S169-S170 ◽  
Author(s):  
C. Sanjurjo Rodriguez ◽  
R. Castro Viñuelas ◽  
T. Hermida Gomez ◽  
I. Fuentes Boquete ◽  
F. De Toro Santos ◽  
...  

Author(s):  
Hoda Keshmiri Neghab ◽  
Mohammad Hasan Soheilifar ◽  
Gholamreza Esmaeeli Djavid

Abstract. Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inflammatory responses, respectively. Vitamin A (0.1–5 μM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inflammation responses.


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