【摘要】：目的探討二氧乳清酸脫氫酶(DHODH)缺失對(duì)線粒體功能和成骨細(xì)胞分化成熟的影響。方法通過特異性小干擾RNA(siRNA)技術(shù)抑制小鼠胚胎成骨細(xì)胞前體細(xì)胞MC3T3-E1細(xì)胞中DHODH表達(dá)后,觀察細(xì)胞增殖、三磷酸腺苷(ATP)產(chǎn)量及骨發(fā)育相關(guān)基因表達(dá)水平。結(jié)果特異性siRNAs降低DHODH表達(dá)后,細(xì)胞增殖受抑制、細(xì)胞周期停滯于G_1/S期。全細(xì)胞ATP產(chǎn)量,特別是線粒體來源的ATP減少。與對(duì)照組相比,DHODH抑制組中Runt相關(guān)轉(zhuǎn)錄因子2(Runx2)及骨鈣素(Ocn)的mRNAs表達(dá)量降低。結(jié)論抑制DHODH蛋白影響成骨細(xì)胞的分化與成熟。成骨細(xì)胞中線粒體功能異�？赡苁菍�(dǎo)致米勒綜合征骨發(fā)育異常的原因之一。
[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.
【作者單位】： 南方醫(yī)科大學(xué)口腔醫(yī)院/廣東省口腔醫(yī)院兒童牙科;廣州醫(yī)科大學(xué)附屬第二醫(yī)院婦科;
【基金】：廣東省自然科學(xué)基金資助項(xiàng)目(2015A030310105) 廣州市衛(wèi)生局醫(yī)藥衛(wèi)生科技項(xiàng)目(20161A011070) 廣州醫(yī)科大學(xué)博士科研啟動(dòng)項(xiàng)目(2014C34)
【分類號(hào)】：R745.43
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本文編號(hào)：2447630