Excessive scar formation in keloids points to altered tissue modeling and repair mechanisms. Dysregulation of cytokine and apoptotic cascades and their downstream signaling pathways might have a role in keloid development. Total RNA was isolated from biopsied keloidal tissue and adjacent normal skin of black patients, white patient's scars, and normal skin of black and white patients, with normal wound healing. Apoptosis, cytokine and NFkB pathway microarrays were used to study and compare gene expression levels. Real-time PCR was used to verify microarray results in original samples and a separate, validation-set of samples. Significant differences were observed in the expression levels of members of caspase, cytokines and MAP kinase pathways, between the normal skin of keloid-prone and normal skin of keloid-resistant patients. Specifically, expression of caspase 6, and caspase 14 genes were different between normal skin of keloid-prone individuals and normal skin of keloid-resistant patients. Our results suggest that normal skin of keloid-prone individuals constitutively expresses a distinct gene profile which might contribute to their susceptibility to develop keloids.
- Gene expression
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