抑制甲基化CpG结合蛋白表达能够诱导人牙周膜成纤维细胞凋亡并降低分化成骨能力  

Inhibition expression of Mecp2 could induce human periodontal ligament fibroblasts apoptosis and reduce osteogenic differentiation capacity

在线阅读下载全文

作  者:陈文君[1] 朱庆勇[1] 沈洋[1] 朱慧[2] 王学富[3] 徐涛[3] 

机构地区:[1]中国人民解放军第105医院口腔科 [2]中国人民解放军第105医院检验科 [3]安徽医科大学药学院

出  处:《中国临床药理学与治疗学》2016年第11期1228-1232,共5页Chinese Journal of Clinical Pharmacology and Therapeutics

基  金:安徽省高校自然科学研究重点项目(KJ2016A348);安徽医科大学博士科研资助基金(XJ201536)

摘  要:目的:探讨甲基化Cp G结合蛋白(Mecp2)在人牙周膜成纤维细胞(h PDLFs)凋亡和分化成骨能力中的作用。方法:通过体外分离并培养人牙周膜成纤维细胞,应用Q-PCR、细胞免疫荧光法和Western blot检测Mecp2在牙周炎h PDLFs中表达变化;并通过siRNA沉默抑制Mecp2表达,使用MTT和流式细胞仪观察对h PDLFs的凋亡和分化成骨能力的作用。结果:细胞免疫荧光结果显示与健康组比较,牙周炎h PDLFs中Mecp2显著低表达;Western blot结果发现Mecp2-siRNA能够明显增加Bax和cleved-caspase-3蛋白表达(P<0.01);细胞流式仪检测发现Mecp2-siRNA能够显著诱导细胞凋亡;同时,Western blot结果还显示Mecp2-siRNA明显降低碱性磷脂酶(ALP)和骨钙素(BGP)蛋白表达。结论:抑制Mecp2表达能够显著诱导h PDLFs细胞凋亡并抑制其分化成骨能力。AIM: To investigate the value of Mecp2 on apoptosis and osteogenic differentiation capacity in human periodontal ligament fibroblasts (hPDLFs). METHODS : After isolated and cul- tured hPDLFs in vitro, the differential expression of Mecp2 was evaluated by immunofluorescence, QPCR and Western blot. With siRNA silencing Mecp2 expression, the use of apoptosis and osteo- genie differentiation was evaluated in hPDLFs by flow cytometry and MTI'. RESULTS: Compared with normal controls, Mecp2 was significantly low- expression in periodontitis hPDLFs by Q-PCR and Western blot. Western blot results showed that Mecp2 could increase Bax and cleved-caspase-3 pro- tein expression ( P 〈 0.01 ). Flow cytometry detected Mecp2-siRNA could significantly induce apopto- sis; similarly, Western blot results of Mecp2-siRNA also showed decreased expression of ALP and BGP. CONCLUSION : Inhibition expression of Mecp2 can significantly increase apoptosis and inhibit differentiation of osteogenic in hPDLFs.

关 键 词:MECP2 人牙周膜成纤维细胞 凋亡 分化 

分 类 号:R965.2[医药卫生—药理学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象