CAJ | 학술논문

目的探讨Follistatin表达抑制对人类骨髓间充质干细胞（BMSC）细胞活性及骨形态发生蛋白（BMP）‐2诱导人类BMSC成骨分化的影响。方法采用 Follistatin特异性 siRNA 转染人类BMSC ，检测线粒体脱氢酶活性、细胞DNA含量及蛋白含量。采用定量逆转录‐聚合酶链式反应（qRT‐PCR）检测成骨相关基因表达，采用碱性磷酸酶（ALP）染色和茜素红染色检测 Follistatin对BMP‐2诱导人类BMSC成骨分化的影响。结果转染后3、7 d ，人类BMSC代谢、DNA含量显著升高；转染后14 d ，总蛋白含量增加。Follistatin表达抑制后成骨相关基因如ALP、OCN、OSX、OC、OPN、RUNX2等表达升高，且ALP活性及钙沉积量显著增加。结论抑制Follistatin表达可促进人类BMSC细胞活性和BMP‐2诱导人类BMSC成骨分化能力，Follistatin可抑制人类BMSC成骨分化。
목적탐토Follistatin표체억제대인류골수간충질간세포（BMSC）세포활성급골형태발생단백（BMP）‐2유도인류BMSC성골분화적영향。방법채용 Follistatin특이성 siRNA 전염인류BMSC ，검측선립체탈경매활성、세포DNA함량급단백함량。채용정량역전록‐취합매련식반응（qRT‐PCR）검측성골상관기인표체，채용감성린산매（ALP）염색화천소홍염색검측 Follistatin대BMP‐2유도인류BMSC성골분화적영향。결과전염후3、7 d ，인류BMSC대사、DNA함량현저승고；전염후14 d ，총단백함량증가。Follistatin표체억제후성골상관기인여ALP、OCN、OSX、OC、OPN、RUNX2등표체승고，차ALP활성급개침적량현저증가。결론억제Follistatin표체가촉진인류BMSC세포활성화BMP‐2유도인류BMSC성골분화능력，Follistatin가억제인류BMSC성골분화。
Objective To investigate the influence of Follistatin depression on bone morphogenetic protein (BMP)‐2‐induced osteogenic differentiation of human bone marrow derived mesenchymal stem cells (BMSCs) and cell viability .Methods Follistatin‐specific small interfering RNA (siRNA) was transfected into human BMSCs ,the mitochondrial dehydrogenase activity ,protein amount and cellular DNA content were measured . The expression levels of some osteoblastic genes were analysed by quantificational reverse transcriptase polymerase chain reaction (qRT‐PCR) ,the influence of Follistatin depression on BMP‐2‐induced osteogenic differentiation of human BMSCs was assessed by alkaline phosphatase (ALP) staining and alizarin red staining .Results Our research indicated that DNA content and human BMSCs metabolism increased remarkably after 3 days and 7 days ,and total protein amount increased after 14 days .The expression levels of ALP ,OCN ,OSX ,OC ,OPN and RUNX2 increased ,ALP activity and calcium deposits increased after Follistatin depression .Conclusion Human BMSC viability and BMP‐2‐induced osteogenic differentiation of human BMSC increases after Follistatin depression , which shows that Follistatin is inhibit factor on osteogenic differentiation of human BMSCs .