Expression of Smad Protein by Normal Skin Fibroblasts and Hypertrophic Scar Fibroblasts in Response to Transforming Growth Factor β1

2008 ◽  
Vol 34 (9) ◽  
pp. 1216-1225 ◽  
Author(s):  
JU-LIN XIE ◽  
SHAO-HAI QI ◽  
SHU PAN ◽  
YING-BIN XU ◽  
TIAN-ZENG LI ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hypertrophic Scar ◽  
Transforming Growth Factor ◽  
Normal Skin ◽  
Transforming Growth Factor Β1 ◽  
Skin Fibroblasts ◽  
Smad Protein

Polymeric Nanofibre Scaffold for the Delivery of a Transforming Growth Factor β1 Inhibitor

2017 ◽  
Vol 70 (3) ◽  
pp. 280 ◽  
Author(s):  
Vipul Agarwal ◽  
Fiona M. Wood ◽  
Mark Fear ◽  
K. Swaminathan Iyer
Keyword(s):  
Tissue Engineering ◽  
Wound Healing ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Normal Skin ◽  
Scar Tissue ◽  
Transforming Growth Factor Β1 ◽  
Collagen I ◽  
Elevated Concentration ◽  
Skin Wound Healing

Skin scarring is a highly prevalent and inevitable outcome of adult mammalian wound healing. Scar tissue is both pathologically and aesthetically inferior to the normal skin owing to elevated concentration of highly orientated collagen I architecture in the innate repaired tissue. With highly invasive surgery being the main treatment modality, there is a great need for alternative strategies to mitigate the problem of scar formation. Tissue engineering approaches using polymeric scaffolds have shown tremendous promise in various disease models including skin wound healing; however, the problem of skin scarring has been greatly overlooked. Herein, we developed an electrospun poly(glycidyl methacrylate) (ES-PGMA) scaffold incorporating a small-molecule antiscarring agent, PXS64. PXS64, a lipophilic neutral analogue of mannose-6-phosphate, has been shown to inhibit the activation of transforming growth factor β1 (TGFβ1). TGFβ1 is a primary protein cytokine regulating the expression of collagen I during wound healing and therefore governs the formation of scar tissue. The nanofibres were tested for biocompatibility as a tissue engineering scaffold and for their efficacy to inhibit TGFβ1 activation in human dermal skin fibroblasts.

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