Dynamic multiphoton imaging of acellular dermal matrix scaffolds seeded with mesenchymal stem cells in diabetic wound healing

2018 ◽  
Vol 11 (7) ◽  
pp. e201700336 ◽  
Author(s):  
Jing Chu ◽  
Panpan Shi ◽  
Xiaoyuan Deng ◽  
Ying Jin ◽  
Hao Liu ◽  
...  
Burns ◽  
2019 ◽  
Vol 45 (7) ◽  
pp. 1685-1694 ◽  
Author(s):  
Yongjun Qi ◽  
Zhengxue Dong ◽  
Hongzhen Chu ◽  
Qi Zhao ◽  
Xiao Wang ◽  
...  

2009 ◽  
Vol 610-613 ◽  
pp. 1298-1301
Author(s):  
Xiang Rong Zhang ◽  
De Wu Liu ◽  
Guang Hua Guo ◽  
Yan Peng

The development of skin tissue engineering provides a noninvasive method for skin restoration. Unfortunately, the lack of a vascular plexus leads to greater time for vascularization compared with native skin autografts and contributes to graft failure. Our purpose was to construct tissue-engineered skin with VEGF- modified human bone marrow mesenchymal stem cells (hMSCs) as well as acellular dermal matrix(ADM) in vitro , Thus by increased vascular endothelial growth factor expression, which could prospectively improve vascularization of tissue-engineered skin for wound healing applications. To reach this aim, hMSCs were isolated and cultured with density gradient centrifugation combined with attachment culture method in vitro. Liposome- mediated gene transfer was used to generate a population of hMSCs overexpressing the gene encoding VEGF165. Then VEGF- modified hMSCs were seeded onto the surface of ADM. The experimental results showed that ADM we prepared has good compatibility with MSCs, the cells in ADM grew and proliferated well in vitro and the tissue - engineered skin with VEGF- modified hMSCs and ADM has been successfully constructed.


2019 ◽  
Vol 312 (5) ◽  
pp. 325-336 ◽  
Author(s):  
Mona Saheli ◽  
Mohammad Bayat ◽  
Rasoul Ganji ◽  
Farzane Hendudari ◽  
Raziyeh Kheirjou ◽  
...  

2009 ◽  
Vol 15 (7) ◽  
pp. 1833-1841 ◽  
Author(s):  
Björn Schönmeyr ◽  
Nicholas Clavin ◽  
Tomer Avraham ◽  
Valerie Longo ◽  
Babak J. Mehrara

2017 ◽  
Vol 49 (10) ◽  
pp. 541-548 ◽  
Author(s):  
Junwang Xu ◽  
Carlos Zgheib ◽  
Maggie M. Hodges ◽  
Robert C. Caskey ◽  
Junyi Hu ◽  
...  

Impaired diabetic wound healing is associated with a dermal extracellular matrix protein profile favoring proteolysis; within the healing diabetic wound, this is represented by an increase in activated matrix metalloproteinase (MMPs). Treatment of diabetic wounds with mesenchymal stem cells (MSCs) has been shown to improve wound healing; however, there has not yet been an assessment of their ability to correct dysregulation of MMPs in diabetic wounds. Furthermore, there has been no prior assessment of the role of microRNA29b (miR-29b), an inhibitory regulatory molecule that targets MMP-9 mRNA. Using in vitro models of fibroblast coculture with MSCs and in vivo murine wound healing models, we tested the hypothesis that MSCs correct dysregulation of MMPs in a microRNA-29b-dependent mechanism. In this study, we first demonstrated that collagen I and III protein content is significantly reduced in diabetic wounds, and treatment with MSCs significantly improves collagen I content in both nondiabetic and diabetic wounds. We then found that MMP-9 gene expression and protein content were significantly upregulated in diabetic wounds, indicating elevated proteolysis. Treatment with MSCs resulted in a decrease in MMP-9 gene expression and protein content level in diabetic wounds 3 and 7 days after wounding. Zymographic analysis indicated that MSC treatment also decreased the amount of activated MMP-9 present in diabetic wounds. Furthermore, miR-29b expression was inversely associated with MMP-9 gene expression; miR-29b expression was decreased in diabetic wounds and diabetic fibroblast. Following treatment of diabetic wounds with MSCs, as well as in diabetic fibroblasts cocultured with MSCs, miR-29b was significantly increased. These findings suggest a potential mechanism through which MSCs enhance diabetic wound healing by improving collagen I content in diabetic wounds through decreasing MMP-9 expression and increasing miR-29b expression.


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