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Updated: Jun 27, 2026
Porcine Model of Infrarenal Abdominal Aortic Aneurysm
Published on: November 21, 2019
Aortic asprosin overexpression does not ameliorate disease pathophysiology in a murine model of Marfan syndrome
Prithviraj Manohar Vijaya Shetty1, Andrea Matzen2,3, Susanne Hille1
1Department of Internal Medicine V, University Hospital Schleswig-Holstein, University of Kiel, German Centre for Cardiovascular Research (DZHK), Partner Site North, Arnold-Heller-Str. 3, 24105, Kiel, Germany.
Abstract:
Marfan syndrome (MFS) is a connective tissue disorder caused by FBN1 mutations, characterised by aortic aneurysms leading to life-threatening dissections. Asprosin is the C-terminal propeptide of fibrillin-1 that was shown to function as a glucogenic hormone with critical implications in vascular pathology. However, its role in MFS remains unknown. Here, we investigate the effect of asprosin overexpression in vascular smooth muscle cells (VSMCs) and in the Marfan mouse model mgR/mgR via endothelial-targeted transduction by adeno-associated viruses (AAVs). In both human and murine VSMCs, asprosin overexpression did not alter VCAM1 or MMP9 expression, while TNF-α-stimulated asprosin-overexpressing MOVAS cells exhibited reduced IL6 levels. In mgR/mgR mice, asprosin overexpression did not affect aortic diameter or elastin integrity. Molecular analyses revealed no significant change in inflammatory or epithelial-to-mesenchymal transition (EMT) markers at the mRNA or protein level, with VCAM1 and MMP9 remaining unchanged. Together, these findings indicate that asprosin overexpression does not ameliorate the aneurysmal phenotype in MFS.
Insights
Asprosin overexpression does not improve aortic aneurysms in Marfan syndrome (MFS). This study found no beneficial effect of asprosin on vascular integrity or disease markers in MFS models.
Area of Science:
- Cardiovascular Biology
- Genetics
- Molecular Medicine
Background:
- Marfan syndrome (MFS) is a genetic connective tissue disorder linked to FBN1 mutations, often causing fatal aortic dissections.
- Asprosin, a fibrillin-1 peptide, acts as a hormone impacting vascular pathology, but its role in MFS is unexplored.
Purpose of the Study:
- To investigate the impact of asprosin overexpression on vascular smooth muscle cells (VSMCs) and a Marfan mouse model.
- To determine if asprosin can mitigate the aneurysmal phenotype characteristic of MFS.
Main Methods:
- Overexpression of asprosin in human and murine VSMCs and in the Marfan mouse model (mgR/mgR) using adeno-associated viruses (AAVs).
- Analysis of VCAM1, MMP9, IL6, inflammatory markers, and epithelial-to-mesenchymal transition (EMT) markers at mRNA and protein levels.
Main Results:
- Asprosin overexpression did not alter VCAM1 or MMP9 expression in VSMCs.
- In Marfan mice, asprosin did not affect aortic diameter, elastin integrity, or key molecular markers of inflammation and EMT.
- Reduced IL6 levels were observed in TNF-α-stimulated asprosin-overexpressing MOVAS cells.
Conclusions:
- Asprosin overexpression does not ameliorate the aneurysmal phenotype in Marfan syndrome.
- The findings suggest asprosin is not a therapeutic target for improving vascular outcomes in MFS.
