OBJECTIVE: To study the potential signal pathway involved in pathogenesis of hypertrophic scar formation. METHODS: The samples of scar were obtained from patients with burn wound scars 6 - 28 months post-burn, while the samples of normal control skin came from the donor site of the same patients. Immunohistochemistry and light microscopy techniques were used to identify the expression of epidermal growth factor receptor (EGFR) and phosphotyrosine proteins (p-Tyr), as well as the phosphorylation of signal transducer and activator of transcription 3 (Stat3) in both hypertrophic scars (n = 6) and normal skin (n = 6). RESULTS: Significant differences were observed in the p-Tyr and EGFR positive expression keratinocytes both in hypertrophic scars and normal skin. The expression of p-Tyr, EGFR and Stat3 protein was greater in hypertrophic scars than in normal skin. However, there was no significant difference in p-Stat3 expression between scar tissues and normal skin. CONCLUSION: Different tyrosine kinase activity occurs in hypertrophic scars and normal cutaneous tissues. Initially, varied expression of EGFR is due to different ligand stimulations. However, phosphotyrosine protein and Stat3 are subsequently activated through phosphorylation. In scar tissues, although EGFR has an intrinsic tyrosine kinase activity when activated by EGFR correlated ligand, phosphorylation of Stat3 showed no significant changes. Therefore, cellular signal pathways are induced by EGFR, which might play a role in hypertrophic scar pathogenesis.
OBJECTIVE: To study the potential signal pathway involved in pathogenesis of hypertrophic scar formation. METHODS: The samples of scar were obtained from patients with burn wound scars 6 - 28 months post-burn, while the samples of normal control skin came from the donor site of the same patients. Immunohistochemistry and light microscopy techniques were used to identify the expression of epidermal growth factor receptor (EGFR) and phosphotyrosine proteins (p-Tyr), as well as the phosphorylation of signal transducer and activator of transcription 3 (Stat3) in both hypertrophic scars (n = 6) and normal skin (n = 6). RESULTS: Significant differences were observed in the p-Tyr and EGFR positive expression keratinocytes both in hypertrophic scars and normal skin. The expression of p-Tyr, EGFR and Stat3 protein was greater in hypertrophic scars than in normal skin. However, there was no significant difference in p-Stat3 expression between scar tissues and normal skin. CONCLUSION: Different tyrosine kinase activity occurs in hypertrophic scars and normal cutaneous tissues. Initially, varied expression of EGFR is due to different ligand stimulations. However, phosphotyrosine protein and Stat3 are subsequently activated through phosphorylation. In scar tissues, although EGFR has an intrinsic tyrosine kinase activity when activated by EGFR correlated ligand, phosphorylation of Stat3 showed no significant changes. Therefore, cellular signal pathways are induced by EGFR, which might play a role in hypertrophic scar pathogenesis.