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Quantitative Micro-CT Analysis of Aortopathy in a Mouse Model of β-aminopropionitrile-induced Aortic Aneurysm and Dissection
Published on: July 16, 2018
Integrated analyses of Mendelian randomization, eQTL, and single-cell transcriptome identify CCN3 as a potential
Haoyu Ran1, Changying Li1, Syed M Musa Rizvi1
1Department of Cardiothoracic Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Insights
This study identifies potential plasma protein biomarkers for aortic dissection (AD). Downregulated CCN3 protein in AD patients suggests a protective role, potentially linked to cell adhesion and signaling pathways.
Area of Science:
- Biochemistry
- Genetics
- Cardiovascular Research
Background:
- Plasma secretory proteins are implicated in various diseases, including aortic dissection (AD).
- Existing research on plasma protein levels and AD lacks specificity.
- Identifying reliable biomarkers for AD is crucial for early detection and treatment.
Purpose of the Study:
- To explore plasma secretory proteins as potential diagnostic biomarkers for aortic dissection (AD).
- To identify specific genes and their protein products associated with AD risk.
- To investigate the functional role of identified proteins in AD pathogenesis.
Main Methods:
- Genome-wide association studies (GWAS) and expression quantitative trait locus (eQTL) analysis.
- Human plasma protein profiling and single-cell RNA sequencing.
- Quantitative PCR (qPCR) for mRNA analysis and ELISA for protein quantification.
Main Results:
- Identified high-risk genes (DBNL, NPC2, SUMF2, TFPI) and low-risk genes (CCN3, PRKCSH, TEX264, TGFBR3) for AD.
- CCN3 showed consistent downregulation in both mRNA and plasma levels in AD patients.
- Enrichment analysis suggested CCN3's involvement in focal adhesion and PI3K-Akt signaling.
Conclusions:
- CCN3 may serve as a protective factor in aortic dissection.
- Downregulation of CCN3 in AD is associated with altered cellular functions.
- Further research into CCN3's role could lead to novel therapeutic strategies for AD.
Abstract:
Plasma secretory proteins are associated with various diseases, including aortic dissection (AD). However, current research on the correlation between AD and plasma protein levels is scarce or lacks specificity. This study aimed to explore plasma secretory proteins as potential biomarkers for AD. Through genome-wide association studies, expression quantitative trait locus (eQTL) analysis, and human plasma protein profiling, we identified DBNL, NPC2, SUMF2, and TFPI as high-risk genes and CCN3, PRKCSH, TEX264, and TGFBR3 as low-risk genes for AD. Further cell localization and differential expression analysis of these eight genes were conducted using single-cell data. We also examined their expression in three Gene Expression Omnibus datasets, measured their mRNA levels in AD versus normal tissues using qPCR, and assessed their protein levels in patients' blood versus healthy individuals using enzyme-linked immunosorbent assay. Our findings suggest that CCN3, consistently downregulated in both mRNA and plasma levels during AD, may have a protective role. Initial enrichment analyses of differentially expressed CCN3 cells suggested their involvement in focal adhesion, actin cytoskeleton regulation, and the PI3K-Akt signaling pathway.
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