Abstract: Objective Keloids are benign fibroproliferative dermal tumors developing as a result of pathological wound healing responses. The key alterations responsible for the pathogenesis of keloids are still poorly understood and there is no satisfactory treatment for this disorder. This study sought to elucidate the pathogenesis of keloid from the aspect of PTGS2 alteration and to find out potential targets for therapy. Methods Skin fibroblasts, the major inductive cell for keloid formation, were transfected with a recombinant PTGS2 siRNA expression vector. Real-time RT-PCR was used to confirm the knock down efficacy of PTGS2 siRNA. We performed gene expression analysis of the fibroblasts transfected with PTGS2 siRNA expression vector in comparison with the fibroblasts transfected with control vector using cDNA microarray chip which comprised of 21,552 clones. Different expression genes were annotated with literature mining method. Results The results of real-time RT-PCR indicated that recombinant PTGS2 siRNA expression vector could significantly knock down the expression of PTGS2 gene. We observed differential regulation of approximately 189 genes of the 10,682 efficient genes data in cDNA microarray，according to the data-filter-standard of 1.5 fold, of which 115 genes were up-regulated and 74 genes were down-regulated when compared with control. 14 genes were differently expressed between transfected fibroblast and control according to the standard of 2 fold, of which 9 genes were up-regulated and 5 genes were down-regulated. Conclusions The results imply that PTGS2 is one of the key alterations responsible for keloid formation and that PTGS2 provide a potential target for therapy of keloid.

Key words: keloid, PTGS2, siRNA, cDNA microarray