Background: A keloid results from excessive collagen deposition, the cause of which remains elusive. A thorough understanding of the pathophysiology of keloid tissue can help determine the most appropriate treatment strategy.
Objectives: To assess the differences in gene expression between keloids and adjacent normal skin in order to define the genes involved in keloid formation.
Methods: Three Korean patients with keloids underwent excision of the keloid and adjacent normal skin, which was used as the control. We investigated expression patterns of genes in the keloids and the normal skin using cDNA microarray and in situ hybridization techniques.
Results: Nine genes in the keloid tissue were consistently upregulated over the 2.0 ratio compared with the normal control from the cDNA microarray composed of 3063 clones: collagen type I alpha1 (NM_000088), DNA segment on chromosome 21 (unique) 2056 expressed sequence (D21S2056E, NNP-1, NM_003683), suppressor of Ty 5 homologue (NM_003169), phosphoglycerate dehydrogenase (NM_032692), adenosine triphosphate synthase beta (NM_001686), serine (or cysteine) proteinase inhibitor, clade H (heat shock protein 47, NM_001235), LIV-1 protein, oestrogen regulated (LIV-1, NM_012319), interleukin-11 receptor alpha (IL11RA, NM_004512) and carbonyl reductase 3 (CBR3, NM_001236). From the in situ hybridization study, the staining signals in the keloid tissue hybridized with anti sense probes of NNP-1 mRNA were stronger than signals in normal controls. Further, endothelial epithelium, but not the epidermis, expressed the signal equally in both keloid and normal control tissue.
Conclusions: We identified nine upregulated genes in keloid tissue using cDNA microarray. Of the nine, the NNP-1 gene was confirmed by topological information using the in situ hybridization technique. We conclude that these nine genes, especially NNP-1, probably contribute either directly or indirectly to keloid formation.