Distinct RNA transcriptome patterns are potentially associated with angiogenesis in Tie2-expressing monocytes
Distinct RNA transcriptome patterns are potentially associated with angiogenesis in Tie2-expressing monocytes
复制标题
独特的 RNA 转录组模式可能与表达 Tie2 的单核细胞中的血管生成相关
DOI:
10.1016/j.gene.2015.12.065
复制
发表时间:
2016-04-10
期刊:
影响因子:
3.5
通讯作者:
Wang, Xipeng
中科院分区:
文献类型:
--
作者:
Wang, Xinjing;Dai, Zhiyuan;Wang, Xipeng
Tie2-expressing Monocytes (TEMs) were previously identified as a novel subset of monocytes and were believed to have prominent pro-angiogenesis activities in human tumors. While the molecular mechanism of the angiogenesis promoting capacity of TEMs remains unclear. RNA transcriptome pattern, including non-coding RNAs as microRNA (miRNA) and long non-coding RNA (IncRNA), plays important role in cell differentiation and functions. However, little is known about the transcriptome patterns of TEMs, including those non-coding RNAs. We explore the transcriptome of TEMs and the matched monocytes that do not express Tie2 (Tie2(-) monocytes) isolated from peripheral blood of healthy adults employing the Agilent Human miRNA(8*60K,Design ID: 046064)microarray and the Agilent IncRNA Gene Expression(4*180K, Design ID: 042818)microarray. A total of 141 mRNAs, 142 IncRNAs and 75 miRNAs were found dysregulated in TEMs compared to Tie2(-) monocytes. TEMs have the distinct RNA transcriptome patterns according to the Hierarchical clustering and then the gene expression patterns were confirmed by quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). Functional annotation by Gene Ontology (GO) analyses showed that the up-regulated mRNAs in TEMs were associated to blood vessel remodeling and positive regulation of epithelial cell proliferation, and the up-regulated insulin like growth factor 1 (IGF1) mRNA was involved in both pathways. For functional analysis of those dysregulated non-coding RNAs, target genes of the miRNAs were predicted and cis/trans-regulation analysis of the IncRNAs were performed. (C) 2016 Elsevier B.V. All rights reserved.