【摘要】：目的獲得肥大心肌細(xì)胞來源外泌體與正常心肌細(xì)胞來源外泌體差異表達(dá)microRNA,并進(jìn)行靶基因和信號通路分析,探討差異表達(dá)microRNA調(diào)控心肌肥大的分子機(jī)制。方法取1~3天齡Wistar新生鼠心臟行原代心肌細(xì)胞培養(yǎng),并分成兩組,模型組用AngⅡ(1μmol/L)誘導(dǎo)心肌細(xì)胞肥大,對照組細(xì)胞未給予任何處理或加入培養(yǎng)液,分離純化上述兩組細(xì)胞外泌體,采用microRNA測序技術(shù)篩選差異表達(dá)microRNA,通過miRanda算法分析差異表達(dá)microRNA靶基因,并行KEGG pathway分析。結(jié)果與對照組比較,肥大心肌細(xì)胞來源外泌體有14個差異表達(dá)microRNA,其中13個microRNA上調(diào)(包括mmu-miR-2137、mmu-miR-5126、mmu-miR-690和10個新發(fā)現(xiàn)的microRNA),1個microRNA下調(diào)(P0.05)。通過miRanda算法得到差異表達(dá)microRNA的靶基因54條,采用排序前20的靶標(biāo)基因及其相關(guān)microRNA構(gòu)建局部網(wǎng)絡(luò)圖。經(jīng)KEGG通路分析發(fā)現(xiàn),差異表達(dá)microRNA參與了MAPK信號通路、PI3K-Akt信號通路、Wnt信號通路等的調(diào)節(jié)。結(jié)論肥大心肌細(xì)胞來源外泌體microRNA表達(dá)譜發(fā)生明顯變化,并經(jīng)靶基因調(diào)節(jié)MAPK等多種信號通路,進(jìn)而影響心肌肥大的病理生理過程。
[Abstract]:Objective to obtain differential expression of microRNA, from exocrine from hypertrophic cardiomyocytes and normal cardiac myocytes, and analyze the target gene and signal pathway to explore the molecular mechanism of differential expression of microRNA in regulating myocardial hypertrophy. Methods Primary cardiomyocytes were cultured in the hearts of 1-day old Wistar neonatal rats and divided into two groups. In the model group, cardiomyocyte hypertrophy was induced by Ang 鈪，

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