DHODH缺失对线粒体功能和成骨细胞分化成熟影响的研究
发布时间：2019-03-26 14:20
【摘要】：目的探讨二氧乳清酸脱氢酶(DHODH)缺失对线粒体功能和成骨细胞分化成熟的影响。方法通过特异性小干扰RNA(siRNA)技术抑制小鼠胚胎成骨细胞前体细胞MC3T3-E1细胞中DHODH表达后,观察细胞增殖、三磷酸腺苷(ATP)产量及骨发育相关基因表达水平。结果特异性siRNAs降低DHODH表达后,细胞增殖受抑制、细胞周期停滞于G_1/S期。全细胞ATP产量,特别是线粒体来源的ATP减少。与对照组相比,DHODH抑制组中Runt相关转录因子2(Runx2)及骨钙素(Ocn)的mRNAs表达量降低。结论抑制DHODH蛋白影响成骨细胞的分化与成熟。成骨细胞中线粒体功能异常可能是导致米勒综合征骨发育异常的原因之一。
[Abstract]:Objective to investigate the effects of (DHODH) deletion of dioxywhey dehydrogenase on mitochondrial function and differentiation and maturation of osteoblasts. Methods the expression of DHODH in mouse embryonic osteoblast precursor cells (MC3T3-E1) was inhibited by specific small interference RNA (siRNA) technique. Cell proliferation, adenosine triphosphate (ATP) production and bone development related gene expression were observed. Results after down-regulation of DHODH expression by specific siRNAs, the cell proliferation was inhibited and the cell cycle was stagnated in G _ (1 / S) phase. The production of whole-cell ATP, especially mitochondrial ATP, decreased. Compared with the control group, the expression of Runt-related transcription factor 2 (Runx2) and osteocalcin (Ocn) mRNAs in the DHODH inhibition group was lower than that in the control group. Conclusion inhibition of DHODH protein affects the differentiation and maturation of osteoblasts. Abnormal mitochondrial function in osteoblasts may be one of the causes of abnormal bone development in Hans Muller's syndrome.
【作者单位】： 南方医科大学口腔医院/广东省口腔医院儿童牙科;广州医科大学附属第二医院妇科;
【基金】：广东省自然科学基金资助项目(2015A030310105) 广州市卫生局医药卫生科技项目(20161A011070) 广州医科大学博士科研启动项目(2014C34)
【分类号】：R745.43
，
本文编号：2447630
[Abstract]:Objective to investigate the effects of (DHODH) deletion of dioxywhey dehydrogenase on mitochondrial function and differentiation and maturation of osteoblasts. Methods the expression of DHODH in mouse embryonic osteoblast precursor cells (MC3T3-E1) was inhibited by specific small interference RNA (siRNA) technique. Cell proliferation, adenosine triphosphate (ATP) production and bone development related gene expression were observed. Results after down-regulation of DHODH expression by specific siRNAs, the cell proliferation was inhibited and the cell cycle was stagnated in G _ (1 / S) phase. The production of whole-cell ATP, especially mitochondrial ATP, decreased. Compared with the control group, the expression of Runt-related transcription factor 2 (Runx2) and osteocalcin (Ocn) mRNAs in the DHODH inhibition group was lower than that in the control group. Conclusion inhibition of DHODH protein affects the differentiation and maturation of osteoblasts. Abnormal mitochondrial function in osteoblasts may be one of the causes of abnormal bone development in Hans Muller's syndrome.
【作者单位】： 南方医科大学口腔医院/广东省口腔医院儿童牙科;广州医科大学附属第二医院妇科;
【基金】：广东省自然科学基金资助项目(2015A030310105) 广州市卫生局医药卫生科技项目(20161A011070) 广州医科大学博士科研启动项目(2014C34)
【分类号】：R745.43
，
本文编号：2447630
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