scholarly journals Human In Vitro Model Mimicking Material‐Driven Vascular Regeneration Reveals How Cyclic Stretch and Shear Stress Differentially Modulate Inflammation and Matrix Deposition

2020 ◽  
Vol 4 (6) ◽  
pp. 1900249 ◽  
Author(s):  
Eline E. Haaften ◽  
Tamar B. Wissing ◽  
Nicholas A. Kurniawan ◽  
Anthal I. P. M. Smits ◽  
Carlijn V. C. Bouten
2003 ◽  
Vol 9 (2) ◽  
pp. 233-241 ◽  
Author(s):  
Dara Chafik ◽  
David Bear ◽  
Phong Bui ◽  
Arush Patel ◽  
Neil F. Jones ◽  
...  

1998 ◽  
Vol 31 ◽  
pp. 173 ◽  
Author(s):  
O. Boutherin Falson ◽  
C. Haond ◽  
M. Chaslon ◽  
M. Moenner ◽  
S. Naili ◽  
...  

1996 ◽  
Vol 800 (1 The Abdominal) ◽  
pp. 270-273 ◽  
Author(s):  
M. M. THOMPSON ◽  
A. WILLS ◽  
E. McDERMOTT ◽  
M. CROWTHER ◽  
N. BRINDLE ◽  
...  

Author(s):  
Peter C. Stubenrauch ◽  
Erin T. Danielson ◽  
Joshua A. Robertson ◽  
Ann M. Kelly ◽  
Stephanie A. Nonas ◽  
...  

2019 ◽  
Author(s):  
Eline E. van Haaften ◽  
Tamar B. Wissing ◽  
Nicholas A. Kurniawan ◽  
Anthal I.P.M. Smits ◽  
Carlijn V.C. Bouten

1AbstractResorbable synthetic scaffolds designed to regenerate living tissues and organs inside the body emerge as a clinically attractive technology to replace diseased blood vessels. However, mismatches between scaffold design and in vivo hemodynamic loading (i.e., cyclic stretch and shear stress) can result in aberrant inflammation and adverse tissue remodeling, leading to premature graft failure. Yet, the underlying mechanisms remain elusive. Here, a human in vitro model is presented that mimics the transient local inflammatory and biomechanical environments that drive scaffold-guided tissue regeneration. The model is based on the co-culture of human (myo)fibroblasts and macrophages in a bioreactor platform that decouples cyclic stretch and shear stress. Using a resorbable supramolecular elastomer as the scaffold material, it is revealed that cyclic stretch initially reduces pro-inflammatory cytokine secretion and, especially when combined with shear stress, stimulates IL-10 secretion. Moreover, cyclic stretch stimulates downstream (myo)fibroblast proliferation and neotissue formation. In turn, shear stress attenuates cyclic-stretch-induced tissue growth by enhancing MMP-1/TIMP-1-mediated collagen remodeling, and synergistically alters (myo)fibroblast phenotype when combined with cyclic stretch. The findings suggest that shear stress acts as a stabilizing factor in cyclic stretch-induced tissue formation and highlight the distinct roles of hemodynamic loads in the design of resorbable vascular grafts.


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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