scholarly journals The Arteriovenous Loop: Engineering of Axially Vascularized Tissue

2018 ◽  
Vol 59 (3-4) ◽  
pp. 286-299 ◽  
Author(s):  
Annika Weigand ◽  
Raymund E. Horch ◽  
Anja M. Boos ◽  
Justus P. Beier ◽  
Andreas Arkudas

Background: Most of the current treatment options for large-scale tissue defects represent a serious burden for the patients, are often not satisfying, and can be associated with significant side effects. Although major achievements have already been made in the field of tissue engineering, the clinical translation in case of extensive tissue defects is only in its early stages. The main challenge and reason for the failure of most tissue engineering approaches is the missing vascularization within large-scale transplants. Summary: The arteriovenous (AV) loop model is an in vivo tissue engineering strategy for generating axially vascularized tissues using the own body as a bioreactor. A superficial artery and vein are anastomosed to create an AV loop. This AV loop is placed into an implantation chamber for prevascularization of the chamber inside, e.g., a scaffold, cells, and growth factors. Subsequently, the generated tissue can be transplanted with its vascular axis into the defect site and anastomosed to the local vasculature. Since the blood supply of the growing tissue is based on the AV loop, it will be immediately perfused with blood in the recipient site leading to optimal healing conditions even in the case of poorly vascularized defects. Using this tissue engineering approach, a multitude of different axially vascularized tissues could be generated, such as bone, skeletal or heart muscle, or lymphatic tissues. Upscaling from the small animal AV loop model into a preclinical large animal model could pave the way for the first successful attempt in clinical application. Key Messages: The AV loop model is a powerful tool for the generation of different axially vascularized replacement tissues. Due to minimal donor site morbidity and the possibility to generate patient-specific tissues variable in type and size, this in vivo tissue engineering approach can be considered as a promising alternative therapy to current treatment options of large-scale defects.

Author(s):  
Bryce M. Whited ◽  
Matthias C. Hofmann ◽  
Peng Lu ◽  
Christopher G. Rylander ◽  
Shay Soker ◽  
...  

The clinical need for alternatives to autologous vein and artery grafts for small-diameter vascular reconstruction have led researches to a tissue-engineering approach. Bioengineered vascular grafts provide a mechanically robust conduit for blood flow while implanted autologous cells remodel the construct to form a fully functional vessel [1]. A typical tissue-engineering approach involves fabricating a vascular scaffold from natural or synthetic materials, seeding the lumen of a vessel with endothelial cells (EC) and the vessel wall with smooth muscle cells or fibroblasts to mimic the functional properties of a native vessel. The cell-seeded vascular scaffold is then preconditioned in vitro using a pulsatile bioreactor to mimic in vivo conditions to enhance vessel maturation before implantation (Fig. 1).


2005 ◽  
Vol 58 (8) ◽  
pp. 1104-1114 ◽  
Author(s):  
S.O.P. Hofer ◽  
G.M. Mitchell ◽  
A.J. Penington ◽  
W.A. Morrison ◽  
R. RomeoMeeuw ◽  
...  

2021 ◽  
Vol 11 ◽  
Author(s):  
Gang Liu ◽  
Qingbai Liu ◽  
Bin Yan ◽  
Ziqiang Zhu ◽  
Yaozeng Xu

Osteoarthritis (OA), the most common form of arthritis, is a very common joint disease that often affects middle-aged to elderly people. However, current treatment options for OA are predominantly palliative. Thus, understanding its pathological process and exploring its potential therapeutic approaches are of great importance. Rat chondrocytes were isolated and exposed to hydrogen peroxide (H2O2) to mimic OA. The effects of H2O2 on ubiquitin-specific protease 7 (USP7) expression, reactive oxygen species (ROS) levels, proliferation, inflammatory cytokine release, and pyroptosis were measured. USP7 was knocked down (KD) or overexpressed to investigate the role of USP7 in OA. Co-immunoprecipitation (Co-IP) was used to study the interaction between USP7 and NAD(P)H oxidases (NOX)4 as well as NOX4 ubiquitination. NOX4 inhibitor was applied to study the involvement of NOX4 in USP7-mediated OA development. USP7 inhibitor was given to OA animals to further investigate the role of USP7 in OA in vivo. Moreover, H2O2 treatment significantly increased USP7 expression, enhanced ROS levels, and inhibited proliferation in rat chondrocytes. The overexpression of USP7 enhanced pyroptosis, ROS production, interleukin (IL)-1β and IL-18 levels, and the expression level of NLRP3, GSDMD-N, active caspase-1, pro-caspase-1, matrix metalloproteinases (MMP) 1, and MMP13, which was abolished by ROS inhibition. The USP7 KD protected rat chondrocytes against H2O2-induced injury. Co-IP results showed that USP7 interacted with NOX4, and USP7 KD enhanced NOX4 ubiquitinylation. The inhibition of NOX4 blocked the pro-OA effect of USP7. Moreover, the USP7 inhibitor given to OA animals suppressed OA in vivo. USP7 inhibited NOX4 ubiquitination for degradation which leads to elevated ROS production. ROS subsequently activates NLPR3 inflammasome, leading to enhanced production of IL-1β and IL-18, GSDMD-N-dependent pyroptosis, and extracellular matrix remodeling. Thus, UPS7 contributes to the progression of OA via NOX4/ROS/NLPR3 axis.


2008 ◽  
Vol 44 (4) ◽  
pp. 806 ◽  
Author(s):  
G. Forte ◽  
Carotenuto F. ◽  
Pagliari F. ◽  
Pagliari S. ◽  
P. Cossa ◽  
...  

Pathobiology ◽  
2013 ◽  
Vol 80 (4) ◽  
pp. 176-181 ◽  
Author(s):  
Meltem Avci-Adali ◽  
Heidi Stoll ◽  
Nadja Wilhelm ◽  
Nadja Perle ◽  
Christian Schlensak ◽  
...  

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