摘要
目的:在牙龈成纤维细胞(gingival fibroblasts(GFs))与牙龈角质形成细胞(gingival kerati-nocytes,GKs)共培养下,研究硝苯地平导致牙龈增生的可能机制。方法:用不同浓度(0、0.2、20μg/mL)硝苯地平处理GFs和GKs的共培养体系,3 d后用逆转录PCR、酶联免疫吸附实验以及流式细胞计数等方法观察角质细胞生长因子(keratinocyte growth factor,KGF)及其受体(keratinocyte growth factor receptor,KGFR)的表达。结果:在共培养条件下,硝苯地平导致GFs表达KGF显著增高,并呈浓度依赖性。同时硝苯地平能促进GKs中KGFR基因表达上调,膜KGFR蛋白表达水平在硝苯地平浓度为0.2μg/mL时上调。结论:间充质-上皮作用途径之一的角质细胞生长因子-受体间相互影响,在硝苯地平导致牙龈增生中起着一定的作用;体外GFs-GKs共培养模型能够在更接近体内环境的状态下进一步研究牙龈增生的机制。
AIM： To explore the possible mechanisms of nifedipine-induced gingival hyperplasia in a gingival fihrohlasts and gingival keratino-cytes co-culture system.METHODS：Gingival fibroblasts（GFs） and keratinocytes（GKs） were isolated and cocultured.With different concentrations（0,0.2,20 μg/mL） of nifedipine treatment on the coculture system,the expression of keratinocyte growth factor（KGF） and keratinocyte growth factor receptor（KGFR） mRNA were examined by reverse transcriptase PCR（RT-PCR）,while the secretion of KGF and the expression of KGFR on the membrane were analyzed by ELISA and flow cytometry,respectively.RESULTS：Under the coculture condition,the expression of KGF in GFs was significantly increased by nifedipine in a dose-dependent manner.Moreover,the expression of KGFR mRNA in GKs was upregulated,and the level of KGFR protein on the membrane was increased when the concentration of nifedipine was 0.2μg/mL.CONCLUSION：The KGF-KGFR pathway of mesenchymal-epithelial interaction plays an important role in the mole cular mechanism of nifedipine-induced gingival hyperplasia.The in vitro coculture model which mimics the in vivo condition can be of great benefit to further study the mechanisms of gingival hyperplasia.
出处
《牙体牙髓牙周病学杂志》
CAS
北大核心
2011年第1期14-18,23,共6页
Chinese Journal of Conservative Dentistry
