本文選題：miR-382 + Porcn��； 參考：《杭州師范大學(xué)》2015年碩士論文

【摘要】：唇腭裂是哺乳動物類先天性遺傳病之一,在我國每700人中就有1人患有此病,屬高發(fā)病。目前,公認(rèn)的致病機(jī)制有有兩方面環(huán)境因素和遺傳因素,大多數(shù)的唇腭裂是由遺傳因素導(dǎo)致。例如,Sox11基因的突變導(dǎo)致小鼠舌頭異常進(jìn)而使得腭板不能正常發(fā)育,以至導(dǎo)致唇/腭裂的產(chǎn)生。因此,闡明唇腭裂的發(fā)病機(jī)制將會促進(jìn)唇腭裂的診斷和修復(fù)。哺乳動物類的腭板發(fā)育進(jìn)程受到嚴(yán)格的分子調(diào)控,包括細(xì)胞增殖、凋亡、遷移以及細(xì)胞類型的轉(zhuǎn)化等。在腭板融合時期涉及到腭板間充質(zhì)細(xì)胞的增殖凋亡及遷移,某些基因翻譯活性受抑制,這時期mRNA翻譯活性受到抑制主要是轉(zhuǎn)錄后調(diào)控機(jī)制調(diào)控,而大部分基因轉(zhuǎn)錄后翻譯抑制受microRNA調(diào)控。我們研究組已驗(yàn)證miR-382在小鼠融合時期表達(dá)量顯著下調(diào),本論文的目的就是要闡明miR-382在小鼠腭板發(fā)育過程中分子機(jī)制。我們研究發(fā)現(xiàn)當(dāng)miR-382在腭板間充質(zhì)細(xì)胞過表達(dá)后,Porcn蛋白表達(dá)明顯下調(diào),通過抑制Porcn(Porcupine)介導(dǎo)促進(jìn)細(xì)胞的遷移,導(dǎo)致下游基因經(jīng)典Wnt通路家族基因如Wnt1、Wnt3和Wnt6等的下調(diào)。miR-382異常表達(dá)可能導(dǎo)致腭板發(fā)育異常。綜上所述,miR-382通過調(diào)控porcn基因調(diào)節(jié)經(jīng)典Wnt通路家族基因的表達(dá),進(jìn)一步影響細(xì)胞的功能。
[Abstract]:Cleft lip and palate is one of the congenital diseases in mammals. At present, there are two kinds of environmental factors and genetic factors, and most of cleft lip and palate are caused by genetic factors. For example, the mutation of Sox11 gene leads to abnormal tongue in mice and leads to abnormal development of palatal plate, leading to lip / cleft palate. Therefore, to clarify the pathogenesis of cleft lip and palate will promote the diagnosis and repair of cleft lip and palate. The development of palatal plate in mammals is regulated by strict molecular regulation, including cell proliferation, apoptosis, migration and cell type transformation. The proliferation, apoptosis and migration of mesenchymal cells in palatine lamina were involved in palatine lamina fusion, and some gene translation activities were inhibited. During this period, the inhibition of mRNA translation activity was mainly regulated by posttranscriptional regulation mechanism. However, most of the gene posttranscriptional inhibition is regulated by microRNA. Our team has demonstrated that the expression of miR-382 is significantly down-regulated during fusion in mice. The aim of this paper is to elucidate the molecular mechanism of miR-382 during the development of palatal plate in mice. We found that the expression of miR-382 protein was down-regulated after overexpression of miR-382 in mesenchymal cells of palatal plate, and promoted cell migration by inhibiting Porcupine. The down-regulation of down-regulated .miR-382 genes in the classical Wnt pathway family of downstream genes, such as Wnt1, Wnt3 and Wnt6, may lead to abnormal palatine plate development. In conclusion, miR-382 regulates the expression of classical Wnt family genes by regulating porcn gene, and further affects cell function.
【學(xué)位授予單位】：杭州師范大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2015
【分類號】：S858.91

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