Changes in Endocan and Dermatan Sulfate Are Associated with Biomechanical Properties of Abdominal Aortic Wall during Aneurysm Expansion and Rupture.

Background and Aims:  The study aimed to assess the potential of proteoglycans (PGs) and collagens as serological biomarkers in the abdominal aortic aneurysm (AAA). Furthermore, we investigated the underlying mechano-biological interactions and signaling pathways.
Methods:  Tissue and serum samples from patients with ruptured AAA (rAAA; n  = 29), elective AAA (eAAA; n  = 78), and healthy individuals ( n  = 8) were evaluated by histology, immunohistochemistry, and enzyme-linked immunosorbent assay, and mechanical properties were assessed by tensile tests. Regulatory pathways were determined by membrane-based sandwich immunoassay.
Results:  In AAA samples, collagen type I and III (Col1 and Col3), chondroitin sulfate, and dermatan sulfate (DS) were significantly increased compared with controls (3.0-, 3.2-, 1.3-, and 53-fold; p  < 0.01). Col1 and endocan were also elevated in the serum of AAA patients (3.6- and 6.0-fold; p  < 0.01), while DS was significantly decreased (2.5-fold; p  < 0.01). Histological scoring showed increased total PGs and focal accumulation in rAAA compared with eAAA. Tissue β-stiffness was higher in rAAA compared with eAAA (2.0-fold, p  = 0.02). Serum Col1 correlated with maximum tensile force and failure tension ( r  = 0.448 and 0.333; p  < 0.01, and r  = 0.02), tissue endocan correlated with α-stiffness ( r  = 0.340; p  < 0.01). Signaling pathways in AAA were associated with extracellular matrix synthesis and vascular smooth muscle cell proliferation. In particular, Src family kinases and platelet-derived growth factor- and epidermal growth factor-related proteins seem to be involved.
Conclusion:  Our findings reveal a structural association between collagen and PGs and their response to changes in mechanical loads in AAA. Particularly Col1 and endocan reflect the mechano-biological conditions of the aortic wall also in the patient's serum and might serve for AAA risk stratification.
Competing Interests: None declared.
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