OBJECTIVEKeloids result from the abnormal repair of the tissues after skin injuries where the pathological overgrowth of large and active fibroblastic cells expands beyond the boundaries of the initiating wound. Imbalanced expression of genes with an as yet unknown regulatory mechanism seems to result in the hypertrophic development of fibroblastic cells and over-productions of collagen. To get information as to genes which function in the actively growing keloid fibroblasts, we have applied a gene expression DNA-microarray technique by analyzing broad range of genes at once in a systematic fashion.

METHODSDifferential gene expressions of keloid fibroblastic cell lines against a normal skin fibroblastic cell line, all of the cell lines had been propagated in our lab, were analyzed using a cDNA-microarray technique. mRNA was extracted from the control normal skin cells and the two lines of keloid fibroblastic cells, one from ear-lobe keloid tissue and the other from chest keloid tissue, was subjected to a DNA microarray analysis which includes 1 100 human genes (TaKaRa Intelli Gene Human CHIP 1K Set I) .

RESULTS8 genes were found to be expressed exclusively in ear-lobe keloid fibroblastic cell lines. Cells from chest keloid were detected to express 17 genes, specifically. Coagulation factor II (thrombin) receptor gene, KIAA0367 protein gene, and matrilin-2 gene were found to be the most commonly expressed genes in the keloid cells. Suppressor genes, like melanoma differentiation associated gene-7, Mda-7 (U16261), were expressed in normal skin fibroblasts but were not expressed in keloid fibroblasts may be implicated in the pathogenesis of the keloid lesions.

CONCLUSIONSGenes expressed specifically in keloid cells may be an adequate pathological diagnostic marker for keloids. Further, Identification of genes that cause cells to develop keloid lesions leads us to gene therapy and prevention of keloids.

Adult ; Cells, Cultured ; Female ; Fibroblasts ; metabolism ; Gene Expression ; Gene Expression Profiling ; Genomics ; Humans ; Keloid ; metabolism ; pathology ; Male ; Oligonucleotide Array Sequence Analysis ; RNA, Messenger ; metabolism

OBJECTIVETo investigate the codon-72 polymorphism of the tumor suppressor gene p53, codon-72 encodes arginine (Arg) or proline (Pro) for a genetic predisposition,to keloid or hypertrophic scar.

METHODSThe distribution of codon 72 polymorphism of p53 gene was analyzed from the 54 keloid and 30 hypertrophic scar(HS)of the Japanese patients with restriction fragment length polymorphism analysis and DNA sequence analysis.

RESULTSThe frequency of the Proline-encoding alleles and Arginine-encoding alleles in the hypertrophic scar patients and the piercing-induced ear-lobe keloid patients, was deviated significantly from that in the normal Japanese controls.

CONCLUSIONSThe Proline-encoding allele and Arginine-encoding allele could have the risks for the hypertrophic scar and the piecing-induced ear-lobe keloid. Also, the pathogenesis of the hypertrophic scar seems to be different from that of keloid at the molecular level.

Cicatrix, Hypertrophic ; genetics ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Humans ; Keloid ; genetics ; Male ; Polymorphism, Genetic ; Tumor Suppressor Protein p53 ; genetics