绝经后骨质疏松患者胎球蛋白-基质gla蛋白-钙磷矿化复合物的作用机制研究

Study on the action mechanism of fetuin A-matrix gla protein-calcium phosphate mineralization complexes in postmenopausal osteoporosis patients

目的探讨胎球蛋白-基质gla蛋白-钙磷矿化复合物（FMC）在绝经后骨质疏松症（PMOP）患者发病中的作用机制。方法分别选择PMOP患者（PMOP组）和骨量正常者（非骨质疏松组）各23名,采用双能X线吸收法（DEXA）测定腰椎骨密度（BMD）,采用酶联免疫吸附试验（ELISA）测定血清胎球蛋白A（fetuin-A）、基质gla蛋白（matrix gla protein,MGP）、骨形态发生蛋白2（bone morphogenetic protein,BMP2）、Runt相关转录因子2（Runt-related transcription factor-2,Run X2）水平,通过聚合酶链式反应（polymerase chain reaction,PCR）检测骨组织局部fetuin A、MGP、BMP2、Run X2mRNA表达。结果 PMOP组血清Fetuin-A、MGP、腰椎BMP2、Run X2 mRNA表达明显低于非骨质疏松组,而腰椎MGPmRNA表达高于非骨质疏松组（P〈0.05）;组间比较,血清BMP2、Run X2水平、腰椎Fetuin-A mRNA表达,均差异无统计学意义（P〉0.05）。多元逻辑回归分析显示,腰椎MGP、BMP2及Run X2 mRNA表达与BMD相关（OR 1.016,95%CI0.809~0.991,P=0.029;OR 1.230,95%CI 1.063~1.424,P=0.015;OR 1.107,95%CI 1.016~1.205,P=0.048）。结论血清FMC合成的减少及MGP在局部骨组织聚集,可能通过影响BMP2/Smad/Run X2信号通路,抑制正常的骨矿化,从而导致PMOP的发生。

Objective To explore the action mechanism of fetuin A-matrix gla protein-calcium phosphate mineralization complexes（ FMC） involved in the pathogenesis of postmenopausal osteoporosis patients（ PMOP）. Methods 23 cases of POMP and 23 cases of non-PMOP were enrolled. DEXA was used to detect lumber bone mineral density（ BMD）,ELISA to measure the level of fetuin-A,MGP,BMP2,Run X2 using. The fetuin A,MGP,BMP2 and Run X2 mRNA expression in local bone tissue were measured by PCR.Results Compared with non-PMOP group,the levels of serum fetuin-A and MGP,the lumbar BMP2 and mRNA expression and Run X2 were significantly lower while mRNA expression of MGP was higher in PMOP group（ P 0. 05）. The level of serum BMP2,Run X2 and lumber mRNA expression of fetuin-A in two groups expressed no statistical significance in comparison between the two groups（ P 0. 05）. Multivariate logistic regression analysis showed that lumbar of MGP, BMP2 mRNA expression and Run X2 correlated with BMD（ OR 1. 016,95% CI 0. 809-0. 991,P = 0. 029; OR 1. 230,95% CI 1. 063-1. 424,P = 0. 015; OR 1. 107,95% CI 1. 016-1. 205,P = 0. 048,respectively）. Conclusion The less synthesis of serum FMC and the aggregation of MGP in local bone tissue may affect the BMP2 / Smad / Run X2 signal pathway and inhibit the normal bone mineralization, thus leading to the occurrence of PMOP.