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Chinese Medical Journal ; (24): 4327-4333, 2013.
Article in English | WPRIM | ID: wpr-327577


<p><b>BACKGROUND</b>Receptor interacting protein 1 (RIP1), which plays a key role in apoptosis, cell survival and programmed cell necrosis, is one of the most important proteins in the RIP family. The purpose of this study was to investigate the roles of RIP1 in the apoptosis, the generation of reactive oxygen species (ROS) and the expression of matrix metalloproteinases (MMPs) induced by ultraviolet B (UVB) in fibroblasts.</p><p><b>METHODS</b>siRNA targeting RIP1 was used to silence RIP1 expression in the NIH3T3 fibroblasts. The mRNA and protein levels of MMP-1 and MMP-3, caspase-3 and -8 activities, and ROS activities were determined by reverse transcriptase-quantitative polymerase chain reaction (RT-qPCR), immunoblotting, caspase activity assay, immunofluorescence, and flow cytometry.</p><p><b>RESULTS</b>The mRNA and protein expressions of MMP-1 and MMP-3 were significantly increased in RIP1 deficient NIH3T3 cells at 24 hours after UVB treatment. At 24 hours after exposure to UVB, RIP1 deficient NIH3T3 cells presented apoptotic morphology, and the apoptosis rate was significantly increased accompanied by pronounced increase in caspase-8 and -3 activities. ROS production was inhibited by UVB at 12 hours in RIP1 deficient NIH3T3 cells.</p><p><b>CONCLUSION</b>RIP1 is involved in NIH3T3 cell damage induced by UVB via participating in the apoptosis, expression of MMPs and ROS production.</p>

Animals , Apoptosis , GTPase-Activating Proteins , Genetics , Metabolism , Matrix Metalloproteinase 1 , Genetics , Metabolism , Matrix Metalloproteinase 3 , Genetics , Metabolism , Matrix Metalloproteinases , Genetics , Metabolism , Mice , NIH 3T3 Cells , RNA, Small Interfering , Reactive Oxygen Species , Metabolism , Ultraviolet Rays
Article in Chinese | WPRIM | ID: wpr-259083


<p><b>OBJECTIVE</b>To evaluate the effect of neuronal differentiation induced by nerve growth factor (NGF) on the tolerance-dosage of ultraviolet radiation of PC12 Cells.</p><p><b>METHODS</b>Neuron-differentiated PC12 cells and untreated PC12 cells were exposed to different ultraviolet radiation dosage of 10, 30, 60, 80, 100, and 200 mJ/cm2. Cell survival rates were determined by MTT assay.</p><p><b>RESULTS</b>Neuron-differentiated PC12 cells had increased tolerance dose to ultraviolet radiation with noticeable apoptosis at the radiation dose of 100 mJ/cm2 in contrast to 30 mJ/cm2 for normal PC12 cells.</p><p><b>CONCLUSION</b>Neuronal differentiation exerts the effect of increasing the tolerance dose of PC12 cells to ultraviolet radiation.</p>

Animals , Cell Differentiation , Cell Transformation, Neoplastic , Radiation Effects , Dose-Response Relationship, Radiation , Nerve Growth Factor , Pharmacology , Neurons , Cell Biology , PC12 Cells , Rats , Ultraviolet Rays
Article in Chinese | WPRIM | ID: wpr-283070


<p><b>OBJECTIVE</b>To investigate the changes in cell proliferation and retinoic acid receptor gamma (RARgamma) mRNA expression in normal human keratinocytes after acitretin treatment and/or narrow-band ultraviolet-B irradiation.</p><p><b>METHODS</b>Normal human keratinocytes were exposed to irradiation with 100 mJ/cm square NB-UVB and/or subsequent 12-hour incubation with 1x10(-6) mol/L acitretin, and the expression of RARgamma mRNA in the cells was examined using RT-PCR and real-time quantitative RT-PCR.</p><p><b>RESULTS</b>A 0.9- and a 2.3-fold increase in RARgamma mRNA expression was induced in the cells by exposure to 100 mJ/cm square NB-UVB and 10(-6) mol/L acitretin, respectively, and the expression was synergistically enhanced by 2.8-fold after their combined treatment.</p><p><b>CONCLUSION</b>Upregulated expression of RARgamma mRNA can be associated with keratinocyte growth inhibition after treatment with acitretin and NB-UVB irradiation.</p>

Acitretin , Pharmacology , Cells, Cultured , Humans , Keratinocytes , Radiation Effects , RNA, Messenger , Metabolism , Receptors, Retinoic Acid , Metabolism , Ultraviolet Rays