ArticleScientific reports2019
Interstitial cells in calcified aortic valves have reduced differentiation potential and stem cell-like properties.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 43 citations in OpenAlex.
- Aortic Stenosis Hyalectan Remodeling Revealed by Proteomics and Glycoproteomics.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Contactin-2 protects against aortic valve calcification via osteogenic differentiation inhibition.Scientific reports · 2026Article
- Infectious seeds of valve calcification: Exploring the bacterial hypothesis in the pathogenesis of calcific aortic valve disease.European journal of clinical investigation · 2026Observational
- The Presence of Adipose Tissue in Aortic Valves Influences Inflammation and Extracellular Matrix Composition in Chronic Aortic Regurgitation.International journal of molecular sciences · 2025Article
- Non-Canonical TERT Activity Initiates Osteogenesis in Calcific Aortic Valve Disease.Circulation research · 2025Article
- Communication between endothelial cells and osteoblasts in regulation of bone homeostasis: Notch players.Stem cell research & therapy · 2025Review
- Insights into preclinical models of calcific aortic valve disease and their translational potential.Frontiers in cardiovascular medicine · 2025Review
- Review
- Oxygenator assisted dynamic microphysiological culture elucidates the impact of hypoxia on valvular interstitial cell calcification.Journal of biological engineering · 2024Article
- Transcriptomic Analysis of Mineralized Adipose-Derived Stem Cell Tissues for Calcific Valve Disease Modelling.International journal of molecular sciences · 2024Article
- Embedding and Backscattered Scanning Electron Microscopy (EM-BSEM) Is Preferential over Immunophenotyping in Relation to Bioprosthetic Heart Valves.International journal of molecular sciences · 2023Article
- Niclosamide Inhibits Aortic Valve Interstitial Cell Calcification by Interfering with the GSK-3β/β-Catenin Signaling Pathway.Biomolecules & therapeutics · 2023Article
- Multicellular aligned bands disrupt global collective cell behavior.Acta biomaterialia · 2023Article
- Reduced Proteolytic Cleavage of von Willebrand Factor Leads to Aortic Valve Stenosis and Load-Dependent Ventricular Remodeling.JACC. Basic to translational science · 2022Article
- High fructose induced osteogenic differentiation of human valve interstitial cells via activating PI3K/AKT/mitochondria signaling.Biomedical journal · 2022Article
- Multi-omics ofFrontiers in cardiovascular medicine · 2022Article
- Uncoupling the Vicious Cycle of Mechanical Stress and Inflammation in Calcific Aortic Valve Disease.Frontiers in cardiovascular medicine · 2022Review
- Models and Techniques to Study Aortic Valve CalcificationFrontiers in pharmacology · 2022Review
- Crenigacestat (LY3039478) inhibits osteogenic differentiation of human valve interstitial cells from patients with aortic valve calcificationFrontiers in cardiovascular medicine · 2022Article
- Shared gene characteristics and molecular mechanisms of macrophages M1 polarization in calcified aortic valve disease.Frontiers in cardiovascular medicine · 2022Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Valve interstitial cells (VICs) are crucial in the development of calcific aortic valve disease. The purpose of the present investigation was to compare the phenotype, differentiation potential and stem cell-like properties of cells from calcified and healthy aortic valves. VICs were isolated from human healthy and calcified aortic valves. Calcification was induced with osteogenic medium. Unlike VICs from healthy valves, VICs from calcified valves cultured without osteogenic medium stained positively for calcium deposits with Alizarin Red confirming their calcific phenotype. Stimulation of VICs from calcified valves with osteogenic medium increased calcification (p = 0.02), but not significantly different from healthy VICs. When stimulated with myofibroblastic medium, VICs from calcified valves had lower expression of myofibroblastic markers, measured by flow cytometry and RT-qPCR, compared to healthy VICs. Contraction of collagen gel (a measure of myofibroblastic activity) was attenuated in cells from calcified valves (p = 0.04). Moreover, VICs from calcified valves, unlike cells from healthy valves had lower potential to differentiate into adipogenic pathway and lower expression of stem cell-associated markers CD106 (p = 0.04) and aldehyde dehydrogenase (p = 0.04). In conclusion, VICs from calcified aortic have reduced multipotency compared to cells from healthy valves, which should be considered when investigating possible medical treatments of aortic valve calcification.
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