摘要
目的:探讨miR-200c对人瘢痕疙瘩成纤维细胞human keloid fibroblasts,HKFs)增殖和胶原合成的影响及阐明其机制。方法:将miR-200c mimics用oligofectami脂质体转染经转化生长因子(TGF)-β1诱导的HKFs,CCK-8法测细胞增殖变化;3H-脯氨酸掺入法测胶原蛋白水平的变化。Western blot检测细胞外信号调节激酶(extracellular signal-regulated kinase,ERK)及磷酸化ERK1/2蛋白表达变化。结果:在有或无TGF-β1刺激下,miR一200c均能明显抑制HKFs的增殖能力及胶原合成,并且能明显减低磷酸化ERK1/2蛋白表达水平,但对非磷酸化ERK表达无影响。结论:miR-200c能抑制HKFs增殖和胶原合成.并起拮抗TGF-B1的作用。其机制可能是通过降低ERK通路活性介导实现的。
Objectives: To investigate the effects of miR-200c on cell proliferation and collagen synthesis in human keloid fibmblasts (HKFs) and elucidate its mechanisms. Methods: HKFs were transfected with miR-200c mimics by oligofectami package. Cell proliferation was assessed by cell counting Kit-8; Rates of collagen synthesis were measured by 3H-proline incorporation assay. Changes of non-phosphorylated ERK and phosphorylated ERK1/2 protein expression were evaluated by Western blot. Results: miR-200e significantly inhibited cell proliferation and collagen synthesis in HKFs with or without TGF-β1 treatment. The expression of phosphorylated ERK1/2 was markedly reduced by miR-200c treatment but non-phos- phorylated ERK expression remained unchanged. Conclusion: miR-200c exhibits inhibitory effects on TGF-β1 and cell proliferation and collagen synthesis in HKFs, and its action mechanisms may be mediated by reducing the ERK pathway activity.
出处
《临床皮肤科杂志》
CAS
CSCD
北大核心
2013年第4期210-213,共4页
Journal of Clinical Dermatology