IN VITRO MODEL OF A HYPERTROPHIC SCAR

Author(s):  
Валериан Сергеевич Шадрин ◽  
Петр Михайлович Кожин ◽  
Олеся Олеговна Шошина ◽  
Александр Леонидович Русанов

Изучение нарушения ранозаживления, приводящего к развитию гиперпластических процессов, является актуальной задачей мирового здравоохранения. Для более детального изучения данной проблематики предложена новая in vitro модель, которая является более удобной для применения и при этом отражает признаки, характерные для гипертрофического рубцевания. The study of wound healing disorders leading to the development of hyperplastic processes is an actual problem of world health. A new in vitro model is proposed for a more detailed study of this problem. This model is more convenient for use and at the same time reflects the signs characteristic of hypertrophic scarring.

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.


2004 ◽  
Vol 12 (2) ◽  
pp. A26-A26
Author(s):  
F E Dhawahir ◽  
C Sheridan ◽  
D Kent ◽  
D Wong ◽  
I Grierson ◽  
...  

2012 ◽  
Vol 44 (4) ◽  
pp. 458 ◽  
Author(s):  
AnilK Balapure ◽  
Jaya Dixit ◽  
Divya Lodha ◽  
Vishal Ranjan ◽  
Ramesh Sharma ◽  
...  

Biomaterials ◽  
2013 ◽  
Vol 34 (28) ◽  
pp. 6695-6705 ◽  
Author(s):  
Sarah Sundelacruz ◽  
Chunmei Li ◽  
Young Jun Choi ◽  
Michael Levin ◽  
David L. Kaplan

1997 ◽  
Vol 110 (7) ◽  
pp. 861-870 ◽  
Author(s):  
D. Greiling ◽  
R.A. Clark

After injury, the wound space is filled with a fibrin/fibronectin clot containing growth factors released by platelets and monocytes. In response to these factors, fibroblasts migrate into the fibrin clot and contribute to the formation of granulation tissue. The functional mechanisms allowing fibroblasts to leave the collagenous matrix of normal connective tissue and invade the provisional matrix of the fibrin clot have not been fully defined. To investigate these mechanisms we established a new in vitro model which simulates specific aspects of early wound healing, that is, the migration of fibroblasts from a three-dimensional collagen matrix into a fibrin clot. This transmigration could be induced by physiological concentrations of platelet releasate or platelet-derived growth factor BB (PDGF-BB) in a concentration-dependent manner. At 24 hours irradiated fibroblasts invaded the fibrin gel almost as well as non-irradiated cells, indicating that transmigration was independent of proliferation. Plasminogen and its activators appear to be necessary for invasion of the fibrin clot since protease inhibitors decreased the amount of migration. These serine proteases, however, were not necessary for exit from the collagen gel as fibroblasts migrated out of the collagen gel onto a surface coated with fibrin fibrils even in the presence of inhibitors. Removal of fibronectin (FN) from either the collagen gel or the fibrin gel markedly decreased the number of migrating cells, suggesting that FN provides a conduit for transmigration. Cell movement in the in vitro model was inhibited by RGD peptide, and by monoclonal antibodies against the subunits of the alpha5 beta1 and alpha v beta3 integrin receptor. Thus, the functional requirements for fibroblast transmigration from collagen-rich to fibrin-rich matrices, such as occurs in early wound healing, have been partially defined using an in vitro paradigm of this important biologic process.


Author(s):  
Chen Fan ◽  
Lay Keng Priscilla Lim ◽  
Zihao Wu ◽  
Bhavya Sharma ◽  
Shi Qi Gan ◽  
...  

2017 ◽  
Vol 27 (5) ◽  
pp. 460-462 ◽  
Author(s):  
Nathalie Deshayes ◽  
Fabienne Bloas ◽  
Florian Boissout ◽  
Jennifer Lecardonnel ◽  
Maryline Paris

2005 ◽  
Vol 55 (1) ◽  
pp. 69-75 ◽  
Author(s):  
Christopher A. Derderian ◽  
Nicholas Bastidas ◽  
Oren Z. Lerman ◽  
Kirit A. Bhatt ◽  
Shin-E Lin ◽  
...  

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