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Isolation of Mouse Interstitial Valve Cells to Study the Calcification of the Aortic Valve In Vitro
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Role for Galectin-3 in Calcific Aortic Valve Stenosis
J Rafael Sádaba1, Ernesto Martínez-Martínez1, Vanessa Arrieta1
1Cardiovascular Translational Research, Navarrabiomed (Miguel Servet Foundation), Instituto de Investigación Sanitaria de Navarra (IdiSNA), Pamplona, Spain.
Journal of the American Heart Association
|November 6, 2016
Summary
Galectin-3 (Gal-3) drives aortic valve calcification in aortic stenosis (AS). Inhibiting Gal-3 in valvular cells reduces inflammatory and osteogenic markers, suggesting a therapeutic target for AS progression.
Area of Science:
- Cardiovascular Biology
- Inflammation and Immunology
- Biomolecular Mechanisms
Background:
- Aortic stenosis (AS) is a chronic inflammatory condition where calcification significantly impacts disease progression.
- Galectin-3 (Gal-3), a pro-inflammatory molecule, is implicated in vascular calcification processes.
- The study investigates the potential role of Gal-3 in mediating aortic valve calcification in AS.
Purpose of the Study:
- To determine if Galectin-3 (Gal-3) mediates aortic valve calcification in patients with aortic stenosis (AS).
- To explore the expression and localization of Gal-3 in human aortic valves (AVs) affected by AS.
- To investigate the in vitro effects of Gal-3 on valvular interstitial cells (VICs) and the impact of Gal-3 inhibition on osteogenic and inflammatory pathways.
Main Methods:
- Analysis of blood samples and aortic valves (AVs) from 77 AS patients and 11 control subjects.
- Immunohistochemical analysis to assess Gal-3 expression and colocalization with cellular and molecular markers.
- In vitro studies using isolated VICs to evaluate Gal-3's role in inflammatory, fibrotic, and osteogenic marker expression via the ERK1/2 pathway.
- Pharmacological inhibition and genetic knockdown of Gal-3 in VICs.
Main Results:
- Galectin-3 (Gal-3) expression was elevated in AVs from AS patients compared to controls.
- Valvular Gal-3 positively correlated with circulating Gal-3 levels and colocalized with VICs, osteogenic, and inflammatory markers.
- In vitro, Gal-3 stimulated inflammatory, fibrotic, and osteogenic markers in VICs through the ERK1/2 pathway.
- Inhibition or knockdown of Gal-3 reduced these markers in differentiated VICs.
Conclusions:
- Galectin-3 (Gal-3) is overexpressed in aortic valves of AS patients and plays a key role in valve calcification.
- Gal-3 inhibition demonstrates potential as a therapeutic strategy to mitigate AS progression.
- Targeting Gal-3 may offer a novel approach to manage aortic valve calcification.
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