Advanced glycation end products on human epidermal keratinocyte cell cycle regulation of mechanisms.docVIP

 PAGE \* MERGEFORMAT 21 Advanced glycation end products on human epidermal keratinocyte cell cycle regulation of mechanisms Of: Dong called cloud, NIU Yi-Wen, Hsieh Ting, youth, Lu Shuliang [Abstract] Objective To investigate the in vitro glycation end products (AGEs) on epidermal keratinocytes in cell cycle regulation in the mechanism. Methods Cultured human epidermal keratinocytes by AGEs (150mg/ml) role, the use of MTT (MTT) method to study the proliferative activity, flow cytometry cell cycle and apoptosis rate. with a small piece of RNA interference (siRNA) method of blocking the receptor cells in AGEs (receptor of AGEs, RAGE) mRNA expression, realtime PCR identification of the blocking efficiency. RT PCR assay before and after blocking RAGE intracellular RAF 1, focal adhesion kinase (FAK), cyclin (cyclin) D1, cyclinB1, the periodic table dependent kinase 4 (CDK4) of the nucleic acid level differential expression. Results AGEs intervention activity of epidermal keratinocyte proliferation decreased, apoptosis increased, the proportion of cell cycle G2 phase was significantly increased, while the cell cycle regulatory factors and signal factors RAF 1, cyclinD1, cyclinB1, CDK4 nucleic acid expression was significantly higher than the control group, with the expression of RAGE is blocked after the above factors, compared with the control group, no difference. Conclusions In this in vitro model, the epidermal keratinocyte cell cycle regulatory factors increased, while proliferation declined and withered death increased AGEs may be activated within cells after the intervention of regulation of endogenous compensatory mechanisms, and this regulatory mechanism and its receptor (RAGE) pathway; AGEs may also above the cell cycle regulatory factors or mechanisms other than the means of biological function. [Keywords:] advanced glycation end products; cyclin D1; cyclin B1; cyclin-dependent kinase 4; cell proliferation Abstract: Objective To explore the mec