CALU polymorphism A29809G affects calumenin availability involving vascular calcification

Jover, Eva; Marín, Francisco; Quintana, Miriam; Pérez-Andreu, Joaquín; Hurtado, José Antonio; Rodrı́guez, Cristina; Martínez-González, José; Gónzález-Conejero, Rocío; Valdés, Mariano; Hernández-Romero, Diana

doi:10.1016/j.yjmcc.2015.03.015

Cited by 16 publications

(14 citation statements)

References 46 publications

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“…Once we confirmed an association between LOX expression and vascular calcification in human tissues, we aimed to corroborate our findings in hVSMCs. We previously reported that the culture of hVSMCs in an osteogenic medium induces ECM calcification and VSMC-to-osteoblast transdifferentiation (9). Results from this study show that HPM-induced calcification in hVSMCs was associated with the up-regulation of COL1A1 and COL1A2 mRNA levels (Fig.…”

Section: Hpm-dependent Calcification Is Associated With the Up-regulasupporting

confidence: 53%

“…Previous studies have demonstrated the ability of HPM to induce ECM mineralization and VSMC-to-osteoblast-like cell transdifferentiation in human cells (9,28). Similarly, HPM promoted a time-dependent extensive calcium deposition in mVSMCs, as demonstrated by colorimetric assessment of calcium and positive Alizarin Red S staining ( Fig.…”

Section: Hpm Induced Calcium Deposition and The Expression Of Osteoblmentioning

confidence: 58%

“…Osteoinduction was performed on VSMCs seeded at 25,000-30,000 cells/cm 2 . Osteogenic high-phosphate medium (HPM) was an adaptation of 2.6 mM HPM (Na 2 HPO 4 /NaH 2 PO 4 , pH 7.4) (9,30) and was carried out after serum starvation for 24 h. All experiments were performed at least 3 times in triplicate or quadruplicate per condition and time point (d). HPM was supplemented with 300 mM of 2,29-dipyridyl (DP) or 500 mM of b-aminopropionitrile (BAPN) (both from MilliporeSigma) to inhibit lysyl hydroxylases (PLOD) (31,32) or LOX (33,34), respectively.…”

Section: Cellular Model For Arterial Calcificationmentioning

confidence: 99%

“…Physiologic osteogenesis shares several commonalities with pathologic ectopic mineralization, including vascular calcification (5,(9)(10)(11)(12)(13)(14)(15). Arterial calcification is an independent risk factor and an established predictor for adverse and disabling cardiovascular events (12,16,17).…”

mentioning

confidence: 99%

“…Furthermore, vascular calcification is one of the main anatomopathological characteristics of advanced and severe atherosclerotic ECM disequilibrium and remodeling (17). Therefore, phenotypic transdifferentiation of vascular cells into osteo/ chondroblast-like cells (6,7,9,10,(18)(19)(20) and active ECM remodeling, including the synthesis of a collagen-enriched matrix and its biomineralization (14,(21)(22)(23)(24), represent the hallmarks of vascular calcification. Diabetes, chronic kidney disease, Coumadin-based anticoagulation, and ageing are also frequently associated with vascular calcification (14).…”

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confidence: 99%

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Inhibition of enzymes involved in collagen cross‐linking reduces vascular smooth muscle cell calcification

et al. 2018

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Vascular smooth muscle cells (VSMCs) transdifferentiate into osteoblast-like cells during vascular calcification, inducing active remodeling and calcification of the extracellular matrix (ECM). Intracellular and extracellular enzymes, such as lysyl hydroxylase 1 (PLOD1) and lysyl oxidase (LOX), contribute to ECM maturation and stabilization. We assessed the contribution of these enzymes to hyperphosphatemia-induced calcification. Human and murine VSMCs were differentiated into functional osteoblast-like cells by high-phosphate medium (HPM) conditioning. HPM promoted ECM calcification and up-regulated osteoblast markers associated with induction of LOX and PLOD1 expression and with an increase in ECM-insoluble collagen deposition. Murine VSMCs from transgenic mice overexpressing LOX (TgLOX) exhibited an increase in HPM-dependent calcification and osteoblast commitment compared with wild-type cells. Similarly, enhanced HPM-induced calcification was detected in aorta from TgLOX. Conversely, β-aminopropionitrile (a LOX inhibitor) and LOX knockdown abrogated VSMC calcification and transdifferentiation. We found a significant positive association between LOX expression and vascular calcification in human atherosclerotic lesions. Likewise, 2,2'-dipyridil (a PLOD inhibitor) and PLOD1 knockdown impaired HPM-induced ECM mineralization and osteoblast commitment. Our findings identify LOX and PLOD as critical players in vascular calcification and highlight the importance of ECM remodeling in this process.-Jover, E., Silvente, A., Marín, F., Martínez-González, J., Orriols, M., Martinez, C. M., Puche, C. M., Valdés, M., Rodriguez, C., Hernández-Romero, D. Inhibition of enzymes involved in collagen cross-linking reduces vascular smooth muscle cell calcification.

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Section: Hpm-dependent Calcification Is Associated With the Up-regulasupporting

confidence: 53%

Section: Hpm Induced Calcium Deposition and The Expression Of Osteoblmentioning

confidence: 58%