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 st...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 norma l skin, which was used as the control. We investigated expression patterns of ge nes in the keloids and the normal skin using cDNA microarray and in situ hybridi zation techniques. Results:Nine genes in the keloid tissue were consistently up -regulated over the 2.0 ratio compared with the normal control from the cDNA microarray composed of 3063 clones:collagen type I αI(NM 000088), DNA segmen t on chromosome 21 (unique) 2056 expressed sequence (D21S2056E, NNP-1, NM 00368 3), suppressor of Ty 5 homologue (NM 003169), phosphoglycerate dehydrogenase (NM 032692), adenosine triphosphatesynthase β(NM 001686), serine (or cysteine) pro teinase inhibitor, clade H (heat shock protein 47, NM 001235), LIV-1 protein, o estrogen regulated (LIV-1, NM 012319), interleukin-11 receptor α(IL11RA, NM 0 04512) and carbonyl reductase 3 (CBR3, NM 001236). From the in situ hybridizatio n study, the staining signals in the keloid tissue hybridized with anti sense pr obes of NNP-1 mRNA were stronger than signals in normal controls. Further, endo thelial epithelium, but not the epidermis, expressed the signal equally in both keloid and normal control tissue. Conclusions:We identified nine upregulated ge nes in keloid tissue using cDNA microarray. Of the nine, the NNP-1 gene was con firmed by topological information using the in situ hybridization technique. We conclude that these nine genes, especially NNP1, probably contribute either dire ctly or indirectly to keloid formation.展开更多
文摘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 norma l skin, which was used as the control. We investigated expression patterns of ge nes in the keloids and the normal skin using cDNA microarray and in situ hybridi zation techniques. Results:Nine genes in the keloid tissue were consistently up -regulated over the 2.0 ratio compared with the normal control from the cDNA microarray composed of 3063 clones:collagen type I αI(NM 000088), DNA segmen t on chromosome 21 (unique) 2056 expressed sequence (D21S2056E, NNP-1, NM 00368 3), suppressor of Ty 5 homologue (NM 003169), phosphoglycerate dehydrogenase (NM 032692), adenosine triphosphatesynthase β(NM 001686), serine (or cysteine) pro teinase inhibitor, clade H (heat shock protein 47, NM 001235), LIV-1 protein, o estrogen regulated (LIV-1, NM 012319), interleukin-11 receptor α(IL11RA, NM 0 04512) and carbonyl reductase 3 (CBR3, NM 001236). From the in situ hybridizatio n study, the staining signals in the keloid tissue hybridized with anti sense pr obes of NNP-1 mRNA were stronger than signals in normal controls. Further, endo thelial epithelium, but not the epidermis, expressed the signal equally in both keloid and normal control tissue. Conclusions:We identified nine upregulated ge nes in keloid tissue using cDNA microarray. Of the nine, the NNP-1 gene was con firmed by topological information using the in situ hybridization technique. We conclude that these nine genes, especially NNP1, probably contribute either dire ctly or indirectly to keloid formation.
