ANALYSIS OF EFFECTS OF MECHANICAL STRESS ON APOPTOSIS OF KELOID DERIVED FIBROBLASTS

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Keloids are characterized by the proliferation of fibroblasts and increased accumulation of extracellular matrix. Excessive growth of fibroblasts and lower rate of apoptosis has been implicated in the etiology of keloids. Malfunction of apoptotic signaling pathways are thought to be one of mechanisms underlying tumorigenic growth of keloid scar. To investigate cellular signaling factors responsible for the malfunction, antimetabolic agents were utilized as an inducer of unusual response in keloid-derived cells. Fibroblasts from keloid skin (KF) and those from normal skin (NF) were compared with respect to their sensitivity to the anti-proliferative effects of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). In KF and NF cells, enhanced levels of p53 and Bax amounts were observed after the treatment. Moreover, human fibroblasts were highly susceptible to apoptosis after mechanical stress exposure by a free-fall. The expression of nuclear p53 and cytoplasmic Bax in the fibroblasts increased at 4 h after mechanical stress exposure. Thus, these molecules may contribute cytotoxic effects of MNNG in KF and NF.