SMAD inhibition attenuates epithelial to mesenchymal transition by primary keratinocytes in vitro

• Published in: Experimental dermatology Vol. 23; no. 7; pp. 497 - 503
• Main Authors: O'Kane, Donal, Jackson, Megan V., Kissenpfennig, Adrien, Spence, Shaun, Damkat-Thomas, Lindsay, Tolland, Julia P., Smyth, Anita E., Denton, Christopher P., Stuart Elborn, J., McAuley, Daniel F., O'Kane, Cecilia M.
• Format: Journal Article
• Language: English
• Published: Denmark Blackwell Publishing Ltd 01.07.2014
• Subjects: Benzamides - chemistry; Collagen - metabolism; Cytokines - metabolism; Dioxoles - chemistry; Down-Regulation; Epidermis - cytology; epithelial to mesenchymal transition; Epithelial-Mesenchymal Transition; Fibronectins - metabolism; Fibrosis - metabolism; Humans; keratinocyte; Keratinocytes - cytology; Matrix Metalloproteinases - metabolism; p38 Mitogen-Activated Protein Kinases - metabolism; Recombinant Proteins - metabolism; Signal Transduction; Smad Proteins - antagonists & inhibitors; Smad Proteins - metabolism; Transforming Growth Factor beta - metabolism; transforming growth factor-β; Tumor Necrosis Factor-alpha - metabolism; tumor necrosis factor-α; Vimentin - metabolism; epithelial to mesenchymal transition; keratinocyte; transforming growth factor-β; tumor necrosis factor-α

Epithelial to mesenchymal transition (EMT) is a process whereby epithelial cells undergo transition to a mesenchymal phenotype and contribute directly to fibrotic disease. Recent studies support a role for EMT in cutaneous fibrotic diseases including scleroderma and hypertrophic scarring, although t...