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1.
Acta Academiae Medicinae Sinicae ; (6): 213-216, 2007.
Article in Chinese | WPRIM | ID: wpr-230001

ABSTRACT

<p><b>OBJECTIVE</b>To explore the effects of antisense epidermal growth factor receptor (EGF-R) oligodeoxynucleotides on ultraviolet-induced c-jun activity of keratinocytes after EGF-R oligodeoxynucleotides transfect to HaCaT in vitro.</p><p><b>METHODS</b>c-jun DNA binding activity after ultraviolet-B (UVB) irradiation and EGF-R oligodeoxynucleotides transfection were determined with a highly sensitive and specific colorimetric method. After EGF-R oligodeoxynucleotides transfection, the mRNA level of EGF-R was detected by reverse transcription polymerase chain reaction method.</p><p><b>RESULTS</b>Compared with control groups, c-jun activity increased significantly in UVB (10, 20, 30 mJ/cm2) irradiation groups (P < 0.05). EGF-R mRNA and c-jun activities induced by UVB were inhibited after the keratinocytes were transfected with EGF-R antisense oligodeoxynucleotides at 2, 4 and 8 microg/ml concentrations (P < 0.01).</p><p><b>CONCLUSION</b>The ultraviolet-induced c-jun activity of keratinocytes can be mediated by EGF-R and inhibited by EGF-R antisense oligodeoxynucleotides, which is transfected to keratinocytes and mediated by lipofectamine.</p>


Subject(s)
Humans , Cell Line , JNK Mitogen-Activated Protein Kinases , Metabolism , Keratinocytes , Metabolism , Radiation Effects , Oligodeoxyribonucleotides, Antisense , Pharmacology , ErbB Receptors , Genetics , Transfection , Ultraviolet Rays
2.
Chinese Medical Journal ; (24): 1838-1841, 2004.
Article in English | WPRIM | ID: wpr-257349

ABSTRACT

<p><b>BACKGROUND</b>It is known that ultraviolet irradiation can affect cellular function through a number of signaling pathways. (-)-epigallocatechin-3-gallate (EGCG) is the major effective component in green tea and can offer protection from ultraviolet-induced damage. In this study, we investigated the protective mechanism of EGCG on human dermal fibroblasts damaged by ultraviolet A (UVA) in vitro.</p><p><b>METHODS</b>Transcription factor Jun protein levels were measured by Western blot. Matrix metalloproteinase 1 (MMP-1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) mRNA were studied by reverse transcription-polymerase chain reaction (RT-PCR) analysis in conjunction with computer-assisted image analysis. MMP-1 and TIMP-1 proteins were quantified by enzyme-linked immunosorbent assay (ELISA).</p><p><b>RESULTS</b>EGCG decreased transcription activity of Jun protein after induction by UVA. Both the mRNA and protein levels of MMP-1 were increased by UVA irradiation, while no significant changes were observed in TIMP-1 levels. The ratio of MMP-1 to TIMP-1 showed statistically significant differences compared with the control. EGCG decreased the ratio of MMP-1 to TIMP-1 by inhibiting UVA-induced MMP-1 expression (P < 0.05).</p><p><b>CONCLUSION</b>EGCG can protect human fibroblasts against UVA damage by downregulating the transcription activity of Jun protein and the expression of MMP-1. The ratio of MMP-1 to TIMP-1, rather than the levels of MMP-1 or TIMP-1 alone, may play a significant role in human skin photodamage.</p>


Subject(s)
Humans , Catechin , Pharmacology , Cells, Cultured , Fibroblasts , Metabolism , Radiation Effects , Gene Expression Regulation , Matrix Metalloproteinase 1 , Genetics , Proto-Oncogene Proteins c-jun , RNA, Messenger , Radiation-Protective Agents , Pharmacology , Reverse Transcriptase Polymerase Chain Reaction , Tissue Inhibitor of Metalloproteinase-1 , Genetics , Ultraviolet Rays
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