Crucial Role of TNF-a in UVB- Induced Apoptosis in the Immortalized Keratinocytes

The deleterious effects of ultraviolet radiation on human skin are via inducing inflammation, immunosuppression, premature skin aging and carcinogenesis. As the most energetic component of ultraviolet radiation reaching the earth’s surface, UVB radiation induces DNA damage and is a critical carcinogenic factor in skin carcinogenesis. However, UVB irradiation may trigger apoptosis and/or cell death by the release of various cytokines in human keratinocytes. Thus, UVB-induced apoptosis and/or cell death may prevent cancer formation. Tumor necrosis factor-a (TNF-a) is suggested to play a role in these responses triggered by UVB, including promoting inflammation, premature skin aging, carcinogenesis, apoptosis and/or cell death. Despite abundant previous studies, however, the mechanism of TNF-a triggering apoptosis has not yet been thoroughly investigated. In this study, the cultured HaCaT cells were irradiated by UVB in graded doses (0-30mJ/cm2). And viability of the HaCaT cells, apoptosis rate and the concentration of tumor neurosis factor-a were tested at 24h post-irradiation. We found that the biological effect of UVB on cell death and /or apoptosis is closely related to the dose. In the small doses range of UVB radiation, the HaCaT apoptosis rate is constantly changing. And those changes may be closely associated with the concentration of TNF-a secreted by HaCaT cells in the culture medium. Between apoptosis rate and the concentration of TNF-a secreted by treated HaCaT cells were positive correlation with linear correlation analysis. Theoretical model of the relationship between TNF-a and apoptosis rate indicated that TNF-a played a crucial role in UVB-induced apoptosis in the immortalized keratinocytes. And TNF-a may also play a part in UVB-triggered necrosis in HaCaT cells.