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骨缺损对脂肪源干细胞骨形态发生蛋白信号通路相关分子的影响
골결손대지방원간세포골형태발생단백신호통로상관분자적영향
Effect of bone defect on expression of molecules related to bone morphogenetic protein signaling pathway in adipose-derived stem cells

万方数据

中华创伤骨科杂志中華創傷骨科雜誌 중화창상골과잡지
CHINESE JOURNAL OF ORTHOPAEDIC TRAUMA
2011年 9期 856-860 ,共5页

余美春%陶晖%杨会营%杨春%曲戎梅%曾文钦%段富华%白宇%戴景兴%原林

여미춘%도휘%양회영%양춘%곡융매%증문흠%단부화%백우%대경흥%원림

成体干细胞%脂肪组织%骨形态发生蛋白受体%骨缺损成體榦細胞%脂肪組織%骨形態髮生蛋白受體%骨缺損
성체간세포%지방조직%골형태발생단백수체%골결손
Adult stem cells%Adipose tissue%Bone morphogenetic protein receptors%Bone defect

目的探讨脂肪源干细胞(ADSCs)是否存在骨形态发生蛋白(BMP)信号通路，以及骨缺损对大鼠内源性ADSCs中BMP信号通路分子表达的影响。方法取30只Wistar大鼠随机分为空白对照组（A组5只）和实验组（B组25只）。A组不做处理，直接取腹股沟脂肪垫进行ADSCs培养。B组制造骨缺损模型，分别于造模后1、3、7、14、21d取腹股沟脂肪组织进行ADSCs培养，每一时间点取5只大鼠。原代培养7d，提取ADSCs总RNA，采用实时定量逆转录聚合酶链反应技术检测BMP受体(BMPR)和Smads的mRNA表达变化。实验数据用95％可信区间表示。结果实验组骨缺损后1、3、7、14、21 d BMPR1a表达量均较对照组明显增加，差异有统计学意义(P＜0.05)；骨缺损后7d表达量(2.532,2.552)增加达高峰。实验组骨缺损后1、3、7、14 d BMPRIb表达量较对照组明显增加，差异有统计学意义(P＜0.05)；骨缺损后14 d表达量(6.628，6.648)增加达高峰。实验组骨缺损3、7、14、21 dBMPR2、Smad5、Smad8表达量较对照组明显增加，差异均有统计学意义(p＜0.05)；骨缺损后14dBMPR2、Smad5表达量(3.538，3.658;8.055,8.149)增加达高峰，骨缺损后3 d Smad8表达量(3.657，3.759)增加达高峰。实验组骨缺损后7、14、21 d Smad1表达量较对照组明显增加，差异均有统计学意义(P＜0.05)；骨缺损后7d表达量(3.641,3.771)增加达高峰。结论 ADSCs表达BMPR，可能存在BMP信号通路，骨缺损可引起大鼠ADSCs中BMP信号通路相关分子的表达增加。
목적탐토지방원간세포(ADSCs)시부존재골형태발생단백(BMP)신호통로，이급골결손대대서내원성ADSCs중BMP신호통로분자표체적영향。 방법취30지Wistar대서수궤분위공백대조조（A조5지）화실험조（B조25지）。A조불주처리，직접취복고구지방점진행ADSCs배양。B조제조골결손모형，분별우조모후1、3、7、14、21d취복고구지방조직진행ADSCs배양，매일시간점취5지대서。원대배양7d，제취ADSCs총RNA，채용실시정량역전록취합매련반응기술검측BMP수체(BMPR)화Smads적mRNA표체변화。실험수거용95％가신구간표시。 결과실험조골결손후1、3、7、14、21 d BMPR1a표체량균교대조조명현증가，차이유통계학의의(P＜0.05)；골결손후7d표체량(2.532,2.552)증가체고봉。실험조골결손후1、3、7、14 d BMPRIb표체량교대조조명현증가，차이유통계학의의(P＜0.05)；골결손후14 d표체량(6.628，6.648)증가체고봉。실험조골결손3、7、14、21 dBMPR2、Smad5、Smad8표체량교대조조명현증가，차이균유통계학의의(p＜0.05)；골결손후14dBMPR2、Smad5표체량(3.538，3.658;8.055,8.149)증가체고봉，골결손후3 d Smad8표체량(3.657，3.759)증가체고봉。실험조골결손후7、14、21 d Smad1표체량교대조조명현증가，차이균유통계학의의(P＜0.05)；골결손후7d표체량(3.641,3.771)증가체고봉。 결론 ADSCs표체BMPR，가능존재BMP신호통로，골결손가인기대서ADSCs중BMP신호통로상관분자적표체증가。
ObjectiveTo investigate the molecules related to bone morphogenetic protein (BMP)signaling pathway in adipose-derived stem cells (ADSCs) and the effects of bone defect on their expression in rat endogenous ADSCs.MethodsThirty Wistar rats were randomly divided into a control group (group A, n =5) and an experimental group (group B, n =25). Rats in group A were not treated before their inguinal adipose pads were used to culture ADSCs. Rats in group B were first made into models of bone defect before their inguinal adipose pads were obtained to culture ADSCs in vitro 1, 3, 7, 14 and 21 days after modeling (5 rats for each time). After 7 days of primary culture, the total RNA was extracted from ADSCs to detect the expressions of BMP receptors and Smads by RT-qPCR.ResultsThe expression of BMPR1awas significantly increased in group B at all time points compared with group A ( P ＜ 0. 05 ), and reached the peak at 7 days after bone defect (2. 532,2. 552). The expression of BMPR1b was significantly increased in group B at 1, 3, 7 and 14 days compared with group A ( P ＜ 0. 05), and reached the peak at 14 days after bone defect (6. 628,6. 648). The expressions of BMPR2, Smad5 and Smad8 were significantly increased in group B at 3, 7, 14 and 21 days compared with group A ( P ＜ 0. 05). The expressions of BMPR2 and Smad5 reached the peak at 14 days after bone defect(3. 538, 3. 658; 8. 055, 8. 149), and the expression of Smad8 reached the peak at 7 days (3. 657,3. 759). The expression of Smad1 was significantly increased in group B at 7, 14 and 21 days compared with group A ( P ＜ 0. 05), and reached the peak at 3 days after bone defect (3. 641,3. 771 ).ConclusionsSince ADSCs can express BMP receptors, there may be a BMP signaling pathway in them. A bone defect may possibly induce an increase in expression of the molecules related to BMP signaling pathway in ADSCs.