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Gene expression in human keloids is altered from dermal to chondrocytic and osteogenic lineage
Author(s) -
Naitoh Motoko,
Kubota Hiroshi,
Ikeda Mika,
Tanaka Toshinori,
Shirane Hirofumi,
Suzuki Shigehiko,
Nagata Kazuhiro
Publication year - 2005
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/j.1365-2443.2005.00902.x
Subject(s) - keloid , biology , sox9 , immunostaining , gene , transcription factor , chondrocyte , gene expression , immunohistochemistry , pathology , microbiology and biotechnology , immunology , cartilage , genetics , anatomy , medicine
Keloids are a dermal fibrotic disease whose etiology remains totally unknown and for which there is no successful treatment. Here, we employed cDNA microarray analysis to examine gene expression in keloid lesions and control skin. We found that 32 genes among the 9000 tested were strongly up‐regulated in keloid lesions, of which 21 were confirmed by Northern blotting. These included at least seven chondrocyte/osteoblast marker genes, and RT‐PCR analysis revealed that transcription factors specific for these genes, SOX9 and CBFA1, were induced. Immunostaining and in situ hybridization further supported that these markers are expressed in keloid lesions. Intriguingly, scleraxis, a transcription factor known as a marker of tendons and ligaments, was also induced in keloid fibroblasts. We propose that reprogramming of gene expression or disordered differentiation from a dermal pattern to that of a chondrocytic/osteogenic lineage, probably closer to that of tendon/ligament lineage, may be involved in the etiology of keloids.