Heat Shock Proteins Modulate Keloid Formation

OBJECTIVE Heat shock proteins (HSPs) modulate the intensity of the inflammatory and synthetic response to stress in wound healing. Induction of HSPs at the site of wounds improves healing by acting as a molecular chaperone. However, the role of HSPs may augment the inflammatory response, leading to an uncontrolled synthetic process. Propensity for keloid development involves genetic predisposition, physical factors, and an aggressive inflammatory response. The aim of this study is to demonstrate the differential expressions of HSPs in keloid and normal tissues. METHODS Twenty-five keloid and adjacent normal tissue samples were removed from 24 patients who were between 16 and 45 years of age. Western blot, enzyme-linked immunosorbent assay, and immunofluorescence studies were performed to examine hsp27, hsp47, hsp60, hsp70, and hsp90 levels in keloid and normal tissue. RESULTS Our results demonstrated a significant overexpression of hsp27, hsp47, and hsp70 in keloid tissue compared to that of normal tissue. Statistical analysis using the Student t test revealed a significant difference between these 2 groups (P < .01), while the expression of hsp60 and hsp90 were not significantly different between the keloid and normal tissue samples. CONCLUSION The overexpression of HSPs indicates that both a proliferative (hsp70) and a matrix synthesis (hsp47, hsp27) component are present in keloid tissue. From this point of view, it is probable that HSPs play a pivotal role in keloid formation. Unveiling HSP-keloid interactions may allow us to manipulate the inflammatory and proliferative phases of wound healing with the potential to control keloid formation.