• Gregor M Bran, Ulrich J Sommer, Ulrich R Goessler, Karl Hörmann, Frank Riedel, and Haneen Sadick.
• Department of Otolaryngology, University Hospital of Mannheim, Theodor-Kutzer-Ufer 1-3, D-68167 Mannheim, Germany. gregor.bran@umm.de
• Anticancer Res. 2010 Sep 1; 30 (9): 3459-63.

AimTo identify the effect of a TGF-β1 antisense treatment of keloid fibroblasts on the SMAD signalling system.Material And MethodsIn this cross-sectional study, keloid and adjacent healthy tissue was harvested from 9 patients with keloid scars after otoplasty. Keloid fibroblasts were placed in monolayer cultures. Expression of SMAD2, -3, -4, -6, and SMURF2 were analysed by immunohistochemistry. Analysis of treatment with antisense oligonucleotides was conducted by immunohistochemistry, and RT-PCR.ResultsImmunohistochemical investigation demonstrated increased expression of SMAD2, -3 and -4, and decreased expression of SMURF2. TGF-β1 antisense therapy significantly down-regulated SMAD2 and SMAD4, up-regulated SMURF2 and showed no effect on SMAD3 and SMAD6.ConclusionTGF-β1 led to elevated levels of the SMAD signalling cascade, indicating an abnormal sensitivity of keloid-derived fibroblasts to this cytokine. Abrogation correlated with potential suppression of the fibro-proliferative progress. There is growing evidence for an abnormal response to this cytokine in the intracellular signal transduction in keloid-derived fibroblasts.

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