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Published on: August 24, 2019
Type A dissection and chronic dilatation: tenascin-C as a key factor in destabilization of the aortic wall
Karola Trescher1, Barbara Thometich, Svitlana Demyanets
1Department of Cardiac Surgery, LK St. Pölten, St. Poelten, Austria. karola.trescher@meduniwien.ac.at
Insights
Tenascin-C is elevated in acute aortic dissection, indicating progressive aortic wall destabilization. This protein may help guide interventions for ascending aorta diseases.
Area of Science:
- Cardiovascular Biology
- Vascular Medicine
- Aortic Disease Research
Background:
- Tenascin-C (TN-C) is implicated in myocardial and vascular remodeling.
- Its role in degenerative diseases of the ascending aorta, including chronic dilatation and acute aortic dissection, requires further elucidation.
Purpose of the Study:
- To investigate the role of tenascin-C in the pathogenesis of chronic dilatation and acute aortic dissection of the ascending aorta.
- To assess tenascin-C expression in aortic tissue and peripheral blood in relation to aortic disease severity.
Main Methods:
- Ascending aortic wall specimens were analyzed from patients with chronic dilatation (n=52), acute Type A dissection (n=30), and controls (n=12).
- Tenascin-C expression was quantified using immunostaining and ImageJ software.
- Peripheral blood TN-C levels were measured via ELISA.
Main Results:
- Tenascin-C staining was homogenous in chronic dilatation and heterogenous/spotty in acute dissection, with no staining in controls.
- Tenascin-C expression was significantly higher in acute Type A dissection compared to chronic dilatation.
- Peripheral blood TN-C levels were elevated in acute dissection but showed no correlation with aortic diameter.
Conclusions:
- Tenascin-C serves as a marker for progressive aortic wall destabilization in both chronic dilatation and acute dissection, independent of aortic size.
- Elevated tenascin-C may be a valuable biomarker for guiding intervention strategies in ascending aorta diseases.
Objectives:
Tenascin-C plays an important role in myocardial and vascular remodelling. We hypothesized that tenascin-C is a key factor in the development of degenerative disease of the ascending aorta, leading to chronic dilatation and acute aortic dissection.
Methods:
Ascending aortic wall specimens were obtained during surgery for chronic dilatation (n=52) and acute Type A dissection (n=30). Patients (n=12) undergoing aortic valve replacement served as controls. Tenascin-C expression was evaluated by immunostaining and semi-quantitatively assessed using the ImageJ software. TN-C levels in peripheral blood were determined by enzyme-linked immunosorbent assay.
Results:
Histological examination showed a clear difference between chronic dilatation and acute dissection. In chronic dilatation, tenascin-C staining was homogenously distributed throughout the media parallel to vascular smooth muscle cells. In acute dissection, a strong staining with a heterogenous and spotty distribution was detected. Control aortas showed no tenascin-C staining. Tenascin-C expression was significantly higher in Type-A dissection compared with chronic dilatation. This was accompanied by a significant elevation of tenascin-C levels in peripheral blood in acute dissection. There was no statistical correlation between the tenascin-C level in peripheral blood and the aortic diameter either in dissection or in dilatation.
Conclusions:
Tenascin-C is a marker of progressive destabilization of the aortic wall independent of size in chronic dilatation and acute dissection. Therefore, it might be a valuable tool in guiding intervention strategies in patients with disease of the ascending aorta.
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