Lin Min, Zhao Lin, Zhao Wenlong, Weng Jing
Department of Neurology, Fuzhou General Hospital of Nanjing Command, PLA, Fuzhou 350025, P.R. China.
Department of Neurosurgery, Fuzhou General Hospital of Nanjing Command, PLA, Fuzhou 350025, P.R. China.
Int J Mol Med. 2014 Dec;34(6):1458-66. doi: 10.3892/ijmm.2014.1960. Epub 2014 Oct 9.
Carotid atherosclerosis is a chronic inflammatory disease of the arterial wall. The present study aimed to identify changes in the gene expression and regulatory factors for atherosclerotic plaques of carotid atherosclerosis from an early to an advanced stage. The original data were downloaded from the NCBI GEO database under accession no. GSE28829. Differentially expressed genes (DEGs) were detected by the Robust Multiarray Average (RMA). The enriched Gene Ontology (GO) terms and pathways for DEGs using DAVID were subsequently identified. The transcriptional and microRNA (miRNA) regulatory network were constructed for the DEGs. Cis-regulatory signals were also investigated. More genes were activated in the advanced stage compared with the early stage. IGHG1 and SPP1 were upregulated, while MYBL1 and PLD were downregulated. The upregulated genes in the advanced stage were involved in atherosclerosis‑related GO terms such as immune, vascular and cell movement homeostasis. The DEGs were significantly enriched in cell adhesion molecules (CAMs) and the focal adhesion pathway. MMP9 and CFL2 played key roles in the transcriptional regulatory network. Moreover, miR-328 was identified as one of the hubs in the miRNA regulatory network. The results may therefore be used to determine the mechanism involved in carotid atherosclerosis.
颈动脉粥样硬化是一种动脉壁的慢性炎症性疾病。本研究旨在确定从早期到晚期颈动脉粥样硬化斑块的基因表达变化和调控因子。原始数据从NCBI GEO数据库下载,登录号为GSE28829。通过稳健多阵列平均法(RMA)检测差异表达基因(DEG)。随后使用DAVID鉴定DEG的富集基因本体(GO)术语和通路。构建了DEG的转录和微小RNA(miRNA)调控网络。还研究了顺式调控信号。与早期相比,晚期有更多基因被激活。IGHG1和SPP1上调,而MYBL1和PLD下调。晚期上调的基因参与了与动脉粥样硬化相关的GO术语,如免疫、血管和细胞运动稳态。DEG在细胞粘附分子(CAM)和粘着斑通路中显著富集。MMP9和CFL2在转录调控网络中起关键作用。此外,miR-328被确定为miRNA调控网络中的枢纽之一。因此,这些结果可用于确定颈动脉粥样硬化的相关机制。