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Comparative tissue proteomics analysis of thoracic aortic dissection with hypertension using the iTRAQ technique
Kefeng Zhang1, Xudong Pan2, Jun Zheng2
1Department of Cardiovascular Surgery, Xuanwu Hospital, Capital Medical University, Beijing, China.
Summary
Researchers identified key proteins in thoracic aortic dissection (TAD) linked to hypertension. These proteins, involved in cell-matrix interactions and inflammation, highlight potential molecular mechanisms driving TAD pathogenesis.
Area of Science:
- Proteomics
- Molecular Biology
- Cardiovascular Research
Background:
- Thoracic aortic dissection (TAD) is a life-threatening condition often associated with hypertension.
- The underlying molecular mechanisms of TAD, particularly in hypertensive individuals, require further elucidation.
- Identifying specific protein alterations in TAD aortic tissue is crucial for understanding disease pathogenesis.
Purpose of the Study:
- To identify differentially expressed proteins in the aortic tissue of patients with thoracic aortic dissection (TAD) and hypertension compared to normal aorta.
- To explore the potential molecular pathogenesis of TAD by analyzing protein expression patterns and associated signaling pathways.
- To validate key identified proteins using western blotting.
Main Methods:
- Proteomic analysis using isobaric tags for relative and absolute quantitation (iTRAQ) on aortic tissue samples from TAD and control groups.
- Bioinformatic analysis of identified proteins and signaling pathways using Metacore software.
- Validation of selected differentially expressed proteins via western blotting.
Main Results:
- A total of 36 differentially expressed proteins were identified, with 19 down-regulated and 17 up-regulated in TAD.
- Key proteins such as fibrillin-1, emilin-1, decorin, protein DJ-1, and histone H4 were validated.
- Enrichment analysis revealed significant involvement of cell-matrix interactions, extracellular matrix (ECM) remodeling, and IL-6 signaling in TAD pathogenesis.
- Evidence of increased transforming growth factor-β (TGF-β) signaling and impaired aortic wall remodeling was observed.
Conclusions:
- Differentially expressed proteins in TAD are primarily associated with cell-matrix interactions, ECM remodeling, and inflammation.
- These molecular mechanisms, potentially influenced by TGF-β signaling, are implicated in the pathogenesis of TAD.
- The findings provide insights into the molecular basis of TAD, offering potential targets for future research and therapeutic strategies.
