Lv Xuejiao, Sun Yuxin, Tan Wenxi, Liu Yang, Wen Naiyan, Fu Shuang, Yu Lanying, Liu Tiantian, Qi Xiaocui, Shu Nanqi, Du Yanwei, Zhang Wenfeng, Meng Yan
Department of Respiratory Medicine and Pathophysiology, Jilin University, No. 218, Ziqiang Road, Nanguan District, Changchun, 130041 Jilin, China.
Department of Otolaryngology, Jilin University, Changchun, Jilin, 130021, China.
Open Life Sci. 2021 Nov 27;16(1):1240-1251. doi: 10.1515/biol-2021-0106. eCollection 2021.
We intended to explore the potential molecular mechanisms underlying the cardiac conduction block inducted by urea transporter (UT)-B deletion at the transcriptome level. The heart tissues were harvested from UT-B null mice and age-matched wild-type mice for lncRNA sequencing analysis. Based on the sequencing data, the differentially expressed mRNAs (DEMs) and lncRNAs (DELs) between UT-B knockout and control groups were identified, followed by function analysis and mRNA-lncRNA co-expression analysis. The miRNAs were predicted, and then the competing endogenous RNA (ceRNA) network was constructed. UT-B deletion results in the aberrant expression of 588 lncRNAs and 194 mRNAs. These DEMs were significantly enriched in the inflammation-related pathway. A lncRNA-mRNA co-expression network and a ceRNA network were constructed on the basis of the DEMs and DELs. The complement 7 (C7)-NONMMUT137216.1 co-expression pair had the highest correlation coefficient in the co-expression network. NONMMUT140591.1 had the highest degree in the ceRNA network and was involved in the ceRNA of NONMMUT140591.1-mmu-miR-298-5p- (GATA binding protein 5). UT-B deletion may promote cardiac conduction block via inflammatory process. The ceRNA NONMMUT140591.1-mmu-miR-298-5p- may be a potential molecular mechanism of UT-B knockout-induced cardiac conduction block.
我们旨在从转录组水平探索尿素转运体(UT)-B缺失诱导心脏传导阻滞的潜在分子机制。从UT-B基因敲除小鼠和年龄匹配的野生型小鼠中采集心脏组织进行长链非编码RNA(lncRNA)测序分析。基于测序数据,鉴定UT-B基因敲除组和对照组之间差异表达的信使核糖核酸(DEM)和lncRNA(DEL),随后进行功能分析和mRNA-lncRNA共表达分析。预测微小核糖核酸(miRNA),然后构建竞争性内源RNA(ceRNA)网络。UT-B缺失导致588个lncRNA和194个mRNA的异常表达。这些DEM在炎症相关途径中显著富集。基于DEM和DEL构建了lncRNA-mRNA共表达网络和ceRNA网络。补体7(C7)-NONMMUT137216.1共表达对在共表达网络中的相关系数最高。NONMMUT140591.1在ceRNA网络中的度数最高,并参与NONMMUT140591.1-小鼠微小核糖核酸-298-5p-(GATA结合蛋白5)的ceRNA过程。UT-B缺失可能通过炎症过程促进心脏传导阻滞。ceRNA NONMMUT140591.1-小鼠微小核糖核酸-298-5p-可能是UT-B基因敲除诱导心脏传导阻滞的潜在分子机制。