發(fā)布時(shí)間：2018-04-01 06:03

  本文選題：SHANK　切入點(diǎn)：誘導(dǎo)性多能干細(xì)胞　出處：《暨南大學(xué)學(xué)報(bào)(自然科學(xué)與醫(yī)學(xué)版)》2017年03期

【摘要】：目的:探索SHANK2基因表達(dá)下調(diào)對(duì)誘導(dǎo)性多能干細(xì)胞神經(jīng)發(fā)育模型的早期影響.方法:體外建立人誘導(dǎo)多能干細(xì)胞來(lái)源的神經(jīng)發(fā)育模型,構(gòu)建攜帶靶向敲減SHANK2基因表達(dá)信息shRNA的慢病毒,在發(fā)育起點(diǎn)感染細(xì)胞模型.在發(fā)育第3、6、9、12、15天分別固定細(xì)胞,熒光顯微鏡拍照,動(dòng)態(tài)監(jiān)測(cè)繼發(fā)于SHANK2表達(dá)下調(diào)的胞體面積、突起長(zhǎng)度與分支、生長(zhǎng)錐面積等神經(jīng)元形態(tài)發(fā)育變化.結(jié)果:體外成功建立人誘導(dǎo)多能干細(xì)胞來(lái)源的神經(jīng)發(fā)育模型.與sh Control組相比,在發(fā)育不同時(shí)間點(diǎn)shSHANK2組神經(jīng)元分支個(gè)數(shù)減少、突起長(zhǎng)度減小,shSHANK2組神經(jīng)元胞體面積、生長(zhǎng)錐面積均有所減小.結(jié)論:SHANK2基因敲減導(dǎo)致早期神經(jīng)元形態(tài)發(fā)育異常,可能是SHANK2導(dǎo)致自閉癥譜系障礙的潛在致病機(jī)制之一.
[Abstract]:Objective: to explore the early effect of down-regulation of SHANK2 gene expression on the neural development of induced pluripotent stem cells. Methods: a human induced neural development model of pluripotent stem cells was established in vitro. To construct a lentivirus carrying shRNA, the expression information of targeted knockdown SHANK2 gene, and to infect the cell model at the beginning of development. The cells were fixed separately on the 15th day of development, and the cells were photographed by fluorescence microscope to dynamically monitor the area of the cell body secondary to the down-regulation of SHANK2 expression. Results: the neuronal development model derived from human pluripotent stem cells was successfully established in vitro. At different time points of development, the number of neuronal branches decreased, the length of process decreased, and the cell body area and growth cone area of shSHANK2 group decreased. Conclusion the knockout of the gene of shSHANK2 group leads to the early morphologic abnormality of neurons. It may be one of the underlying pathogenesis of autism spectrum disorder caused by SHANK2.
【作者單位】： 暨南大學(xué)粵港澳中樞神經(jīng)再生研究院;
【基金】：國(guó)家自然科學(xué)基金項(xiàng)目(31400922)
【分類(lèi)號(hào)】：R749
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本文編號(hào)：1694266