【摘要】 目的探讨miR-222在长波紫外线(UVA)诱导的光老化模型中的调节作用。方法分离并培养人皮肤成纤维细胞(HDFs),用0,2.5,5.0和7.5J不同剂量UVA辐射诱导光老化模型,用实时定量PCR和Western-blot分别检测miR-222和基质金属蛋白酶1(MMP1)的表达情况。用miR-222的功能模拟物和miR-222的功能抑制物分别转染HDFs,检测MMP1表达情况。对HDFs细胞分别转染miR-222功能模拟物、miR-222阴性对照物、miR-222功能抑制物和miR对照的功能抑制物,转染24h后予UVA辐射诱导光老化模型,检测MMP1表达情况。结果 HDFs经不同剂量UVA辐射后,MMP1表达与对照组相比显著升高(P<0.01),同时miR-222表达与对照组相比显著降低(P<0.01)。miR-222转染HDFs后再予UVA辐射,miR-222转染组MMP1表达显著低于miR对照组(t=5.616,P<0.05),而miR-222抑制物转染组MMP1表达与miR对照组相比无显著的改变。结论人皮肤成纤维细胞光老化模型中UVA辐射可导致miR-222表达降低,从而上调MMP1表达。更多还原

【Abstract】 Objective To investigate the effects of miR-222 on ultraviolet A( UVA) induced skin photoaging. Methods The primary human dermal fibroblasts( HDFs) were isolated and cultured. After exposure to different does( 0,2. 5,5. 0 and 7. 5 J/cm2) of UVA,the mR NA and protein levels of metal matrix proteinase 1( MMP1)in HDFs were detected by real-time PCR and Western blot respectively,and the levels of miR-222 was detected by real-time PCR. MiR-222 mimic,miR mimic control,anti- miR-222 and anti- miR mimic control were respectively transfected into HDFs before UVA exposure,and then the protein levels of MMP1 were detected. Results After exposure to UVA,the expression of MMP1 was significantly increased( P < 0. 01),while the levels of miR-222 was significantly decreased( P < 0. 01). When HDFs was exposed to UVA after transfected with miR-222 mimic,the protein levels of MMP1 in miR-222 mimic transfected group was significantly lower than in miR control( P < 0. 05),while there was no difference between anti- miR-222 transfected group and control group. Conclusion UVA could down-regulate the levels of miR-222 thus down-regulating the expression of MMP1 in HDFs photoaging model.更多还原