IGFBP6 Is Downregulated in Unstable Carotid Atherosclerotic Plaques According to an Integrated Bioinformatics Analysis and Experimental Verification
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- Liu Yandong
- Department of Vascular and Endovascular Surgery, Changzheng Hospital Affiliated to the Second Military Medical University
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- Huan Wei
- Department of Vascular and Endovascular Surgery, Changzheng Hospital Affiliated to the Second Military Medical University
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- Zou Sili
- Department of Vascular and Endovascular Surgery, Changzheng Hospital Affiliated to the Second Military Medical University
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- Wu Jianjin
- Department of Vascular and Endovascular Surgery, Changzheng Hospital Affiliated to the Second Military Medical University
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- Qu Lefeng
- Department of Vascular and Endovascular Surgery, Changzheng Hospital Affiliated to the Second Military Medical University
書誌事項
- 公開日
- 2020-10-01
- 資源種別
- journal article
- DOI
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- 10.5551/jat.52993
- 公開者
- 一般社団法人 日本動脈硬化学会
この論文をさがす
説明
<p>Aims: To investigate the differentially expressed genes (DEGs) and molecular interaction in unstable atherosclerotic carotid plaques. </p><p>Methods: Gene expression datasets GSE41571, GSE118481, and E-MTAB-2055 were analyzed. Co-regulated DEGs in at least two datasets were analyzed with the enrichment of Gene Ontology Biological Process (GO-BP), Kyoto Encyclopedia of Genes and Genomes (KEGG), protein–protein interaction (PPI) networks, interrelationships between miRNAs/transcriptional factors, and their target genes and drug–gene interactions. The expression of notable DEGs in human carotid artery plaques and plasma was further identified. </p><p>Results: The GO-BP enrichment analysis revealed that genes associated with inflammatory response, and extracellular matrix organization were altered. The KEGG enrichment analysis revealed that upregulated DEGs were enriched in the tuberculous, lysosomal, and chemokine signaling pathways, whereas downregulated genes were enriched in the focal adhesion and PI3K/Akt signaling pathway. Collagen type I alpha 2 chain (COL1A2), adenylate cyclase 3 (ADCY3), C-X-C motif chemokine receptor 4 (CXCR4), and TYRO protein tyrosine kinase binding protein (TYROBP) might play crucial roles in the PPI networks. In drug–gene interactions, colonystimulating factor-1 receptor had the most drug interactions. Insulin-like growth factor binding protein 6 (IGFBP6) was markedly downregulated in unstable human carotid plaques and plasma. Under a receiver operating characteristic curve analysis, plasma IGFBP6 had a significant discriminatory power (AUC, 0.894; 95% CI, 0.810–0.977), with a cutoff value of 142.08 ng/mL. </p><p>Conclusions: The genes COL1A2, ADCY3, CXCR4, and TYROBP are promising targets for the prevention of unstable carotid plaque formation. IGFBP6 may be an important biomarker for predicting vulnerable plaques.</p>
収録刊行物
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- Ｊｏｕｒｎａｌ ｏｆ Ａｔｈｅｒｏｓｃｌｅｒｏｓｉｓ ａｎｄ Ｔｈｒｏｍｂｏｓｉｓ
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Ｊｏｕｒｎａｌ ｏｆ Ａｔｈｅｒｏｓｃｌｅｒｏｓｉｓ ａｎｄ Ｔｈｒｏｍｂｏｓｉｓ 27 (10), 1068-1085, 2020-10-01
一般社団法人 日本動脈硬化学会
