AI Article Synopsis
- The study aimed to explore how TGF-β1 antisense treatment affects the SMAD signaling system in keloid fibroblasts.
- Keloid and healthy tissue samples from 9 patients were analyzed for the expression of various SMAD proteins using immunohistochemistry and RT-PCR techniques.
- Results showed that TGF-β1 increased the levels of certain SMAD proteins while the antisense therapy decreased some of them, indicating an abnormal response of keloid fibroblasts to TGF-β1 which may contribute to excessive tissue growth.
Article Abstract
Aim: To identify the effect of a TGF-β1 antisense treatment of keloid fibroblasts on the SMAD signalling system.
Material And Methods: In 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.
Results: Immunohistochemical 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.
Conclusion: TGF-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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