ArticleJournal of cellular physiology2017
End stage renal disease-induced hypercalcemia may promote aortic valve calcification via Annexin VI enrichment of valve interstitial cell derived-matrix vesicles.
Article in Journal of cellular physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 71 citations in OpenAlex.
- Calcific aortic valve disease augments vesicular microRNA-145-5p to regulate the calcification of valvular interstitial cells via cellular crosstalk.Basic research in cardiology · 2025Article
- Nutrient restriction protects against valve interstitial cell calcification by upregulating ubiquitin mediated proteolysis.Frontiers in cardiovascular medicine · 2025Article
- Gla Rich Protein (GRP) Mediates Vascular Smooth Muscle Cell (VSMC) Osteogenic Differentiation, Extracellular Vesicle (EV) Calcification Propensity, and Immunomodulatory Properties.International journal of molecular sciences · 2024Article
- Do Media Extracellular Vesicles and Extracellular Vesicles Bound to the Extracellular Matrix Represent Distinct Types of Vesicles?Biomolecules · 2023Review
- Metformin ameliorates valve interstitial cell calcification by promoting autophagic flux.Scientific reports · 2023Article
- Vascular calcification: from the perspective of crosstalk.Molecular biomedicine · 2023Review
- Multiomics of Tissue Extracellular Vesicles Identifies Unique Modulators of Atherosclerosis and Calcific Aortic Valve Stenosis.Circulation · 2023Article
- AnnexinA6: a potential therapeutic target gene for extracellular matrix mineralization.Frontiers in cell and developmental biology · 2023Review
- Review
- PALMD regulates aortic valve calcification via altered glycolysis and NF-κB-mediated inflammation.The Journal of biological chemistry · 2022Article
- MicroRNA-22 promoted osteogenic differentiation of valvular interstitial cells by inhibiting CAB39 expression during aortic valve calcification.Cellular and molecular life sciences : CMLS · 2022Article
- Heat Shock Protein 90 as Therapeutic Target for CVDs and Heart Ageing.International journal of molecular sciences · 2022Review
- Annexins and cardiovascular diseases: Beyond membrane trafficking and repair.Frontiers in cell and developmental biology · 2022Review
- Overexpressed Thrombospondin 2 Induced Osteogenic Differentiation of Valve Interstitial Cells via Inhibition of Akt/NF-Disease markers · 2022Article
- Multi-omics ofFrontiers in cardiovascular medicine · 2022Article
- Models and Techniques to Study Aortic Valve CalcificationFrontiers in pharmacology · 2022Review
- The functional role of soluble proteins acquired by extracellular vesicles.Journal of extracellular biology · 2022Review
- Lipoprotein(a) Induces Vesicular Cardiovascular Calcification Revealed With Single-Extracellular Vesicle Analysis.Frontiers in cardiovascular medicine · 2022Article
- Role of Extracellular Vesicles as Potential Diagnostic and/or Therapeutic Biomarkers in Chronic Cardiovascular Diseases.Frontiers in cell and developmental biology · 2022Review
- Matrix Vesicles as a Therapeutic Target for Vascular Calcification.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 1 country.
Funding
Abstract
Patients with end-stage renal disease (ESRD) have elevated circulating calcium (Ca) and phosphate (Pi), and exhibit accelerated progression of calcific aortic valve disease (CAVD). We hypothesized that matrix vesicles (MVs) initiate the calcification process in CAVD. Ca induced rat valve interstitial cells (VICs) calcification at 4.5 mM (16.4-fold; p < 0.05) whereas Pi treatment alone had no effect. Ca (2.7 mM) and Pi (2.5 mM) synergistically induced calcium deposition (10.8-fold; p < 0.001) in VICs. Ca treatment increased the mRNA of the osteogenic markers Msx2, Runx2, and Alpl (p < 0.01). MVs were harvested by ultracentrifugation from VICs cultured with control or calcification media (containing 2.7 mM Ca and 2.5 mM Pi) for 16 hr. Proteomics analysis revealed the marked enrichment of exosomal proteins, including CD9, CD63, LAMP-1, and LAMP-2 and a concomitant up-regulation of the Annexin family of calcium-binding proteins. Of particular note Annexin VI was shown to be enriched in calcifying VIC-derived MVs (51.9-fold; p < 0.05). Through bioinformatic analysis using Ingenuity Pathway Analysis (IPA), the up-regulation of canonical signaling pathways relevant to cardiovascular function were identified in calcifying VIC-derived MVs, including aldosterone, Rho kinase, and metal binding. Further studies using human calcified valve tissue revealed the co-localization of Annexin VI with areas of MVs in the extracellular matrix by transmission electron microscopy (TEM). Together these findings highlight a critical role for VIC-derived MVs in CAVD. Furthermore, we identify calcium as a key driver of aortic valve calcification, which may directly underpin the increased susceptibility of ESRD patients to accelerated development of CAVD.
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