Enhancement of UVB radiation-mediated apoptosis by knockdown of cytosolic NADP+-dependent isocitrate dehydrogenase in HaCaT cells
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Ultraviolet B (UVB) radiation induces the production ofreactive oxygen species (ROS) that promote apoptotic celldeath. We showed that cytosolic NADP+-dependent isocitratedehydrogenase (IDPc) plays an essential role in the control ofcellular redox balance and defense against oxidative damage,by supplying NADPH for antioxidant systems. In this study, wedemonstrated that knockdown of IDPc expression by RNAinterference enhances UVB-induced apoptosis of immortalizedhuman HaCaT keratinocytes. This effect manifested as DNAfragmentation, changes in cellular redox status, mitochondrialdysfunction, and modulation of apoptotic marker expression. Based on our findings, we suggest that attenuation of IDPcexpression may protect skin from UVB-mediated damage, byinducing the apoptosis of UV-damaged cells.
Abstract
Ultraviolet B (UVB) radiation induces the production ofreactive oxygen species (ROS) that promote apoptotic celldeath. We showed that cytosolic NADP+-dependent isocitratedehydrogenase (IDPc) plays an essential role in the control ofcellular redox balance and defense against oxidative damage,by supplying NADPH for antioxidant systems. In this study, wedemonstrated that knockdown of IDPc expression by RNAinterference enhances UVB-induced apoptosis of immortalizedhuman HaCaT keratinocytes. This effect manifested as DNAfragmentation, changes in cellular redox status, mitochondrialdysfunction, and modulation of apoptotic marker expression. Based on our findings, we suggest that attenuation of IDPcexpression may protect skin from UVB-mediated damage, byinducing the apoptosis of UV-damaged cells.
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