Abbreviations: GAPDH, glyceraldehyde-3-phosphate dehydrogenase; ODC, ornithine decarboxylase A bstract UV radiation is known to cause photoaging of the skin and is considered one of the leading cause of developing skin carcinogenesis. Melatonin w hich has a highly lipophilic m olecular structure facilitating penetration of cell m em branes and serving as an extra-and intracellular free radical scavenger has been dem onstrated to protect photodam age of skin affected by UV exposure. In this study, w e have exam ined the role of m elatonin in response to UVB induced photodam aging process, using hum an skin fibroblasts in vitro.
In a previous study, we established a stable cell line which constitutively expresses E7 in HaCaT human keratinocyte cell line and identified various relevant factors including oxygen modulators affected by the E7 oncogene. E7-expressing HaCaT cells (HaCaT/E7) appeared to be more resistant to H2O2-induced cell death. Here, we demonstrate how E7 oncogene would modulate oxidative stress-induced cell death. In addition, we verified the increased expression of catalase in the HaCaT/E7 by Western blot analysis. The results suggest that the E7 oncogene would induce higher resistance to ROS-induced cell injury in the E7-infected cells via the upregulation of catalase. To investigate these paradoxical effects of high concentrations of H2O2 (500 microM-1 mM), we examined their effects on receptor mediated apoptosis, cell death via the mitochondrial pathway and modulation of apoptosis related factors. Our results revealed that HaCaT keratinocytes infected with HPV 16 E7 oncogene modulated expressions of catalase, Bcl-xL, IL-18, Fas, Bad, and cytochrome c as well as NF-kappaB, resulting in the resistance to oxidative stress-induced cell death.
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