Assay for Human Matrix Gla Protein in Serum

Braam, Lavienja A. J. L. M.; Dissel, P.E.P.; Gijsbers, Birgit L. M. G.; Spronk, Henri M. H.; Hamulyák, Karly; Soute, Berry A.M.; Debie, Wiel H.; Vermeer, Cees

doi:10.1161/01.atv.20.5.1257

Cited by 82 publications

(35 citation statements)

References 21 publications

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“…Furthermore, Braam et al found that levels of circulating MGP in patients with type 1 Diabetes Mellitus (which is a risk factor for atherosclerosis) were elevated [40]. Our findings concerning the group B of patients (CKD patients without diabetes) are in agreement with the results of Jono et al, which detected a reverse association between the levels of serum MGP and coronary artery calcification [9].…”

Section: Discussionsupporting

confidence: 92%

Association of matrix γ-carboxyglutamic acid protein levels with insulin resistance and Lp(a) in diabetes: A cross-sectional study

Antonopoulos

Mylonopoulou²,

Angelidi

et al. 2017

Diabetes Research and Clinical Practice

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Antonopoulos, S.; Mylonopoulou, M.; Angelidi, A.M.; Kousoulis, A.A.; Tentolouris, N. (2017) This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. The detected Lp(a) and MGP association in CKD4 patients may also represent the key to the complicated mechanism of their coexisting accelerated atherosclerosis and vascular calcification. ASSOCIATION OF MATRIX γ-CARBOXYGLUTAMIC ACID PROTEIN LEVELS WITH INSULIN RESISTANCE AND Lp(a) IN DIABETES : A CROSS-SECTIONAL STUDY

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Section: Discussionsupporting

confidence: 92%

Association of matrix γ-carboxyglutamic acid protein levels with insulin resistance and Lp(a) in diabetes: A cross-sectional study

Antonopoulos

Mylonopoulou²,

Angelidi

et al. 2017

Diabetes Research and Clinical Practice

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“…26 In patients with severe atherosclelosis, circulating osteocalcin levels were increased. 27 Another study showed that during atherogenesis, osteocalcin had a regulatory role not only in atherosclerotic calcium but also in osteoclastogenesis. 28 Although osteocalcin might be one of the important factors explaining the relationship between endothelial function and bone mass, the present study found that brachial arterial FMD showed no significant association with osteocalcin concentrations.…”

Section: Discussionmentioning

confidence: 99%

Relationship Between Brachial Arterial Endothelial Function and Lumbar Spine Bone Mineral Density in Postmenopausal Women

Sumino

Ichikawa²,

Kasama³

et al. 2007

Circ J

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“…After blotting, membranes were incubated at 4°C overnight with biotin-conjugated a3-15 MGP IgG or a rabbit polyclonal antibody raised against bovine fetuin (23,24). Visualization was via streptavidin-horseradish peroxidase (Amersham Pharmacia, Uppsala, Sweden) and development with ECL Western blotting detection reagents (Amersham Pharmacia).…”

Section: Western Blot Analysismentioning

confidence: 99%

Human Vascular Smooth Muscle Cells Undergo Vesicle-Mediated Calcification in Response to Changes in Extracellular Calcium and Phosphate Concentrations

Reynolds¹,

Joannides²,

Skepper³

et al. 2004

Journal of the American Society of Nephrology

835

764

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Abstract. Patients with ESRD have a high circulating calcium (Ca) ϫ phosphate (P) product and develop extensive vascular calcification that may contribute to their high cardiovascular morbidity. However, the cellular mechanisms underlying vascular calcification in this context are poorly understood. In an in vitro model, elevated Ca or P induced human vascular smooth muscle cell (VSMC) calcification independently and synergistically, a process that was potently inhibited by serum. Calcification was initiated by release from living VSMC of membrane-bound matrix vesicles (MV) and also by apoptotic bodies from dying cells. Vesicles released by VSMC after prolonged exposure to Ca and P contained preformed basic calcium phosphate and calcified extensively. However, vesicles released in the presence of serum did not contain basic calcium phosphate, co-purified with the mineralization inhibitor fetuin-A and calcified minimally. Importantly, MV released under normal physiologic conditions did not calcify, and VSMC were also able to inhibit the spontaneous precipitation of Ca and P in solution. The potent mineralization inhibitor matrix Gla protein was found to be present in MV, and pretreatment of VSMC with warfarin markedly enhanced vesicle calcification. These data suggest that in the context of raised Ca and P, vascular calcification is a modifiable, cell-mediated process regulated by vesicle release. These vesicles contain mineralization inhibitors derived from VSMC and serum, and perturbation of the production or function of these inhibitors would lead to accelerated vascular calcification.Patients with ESRD develop extensive medial calcification, or Monckeberg's sclerosis, that causes increased arterial stiffness and contributes to the high cardiovascular mortality (1,2). Calciphylaxis is an increasingly common and life-threatening form of calcification characterized by destructive calcification in the media of subcutaneous arterioles, leading to occlusion and subsequent widespread tissue necrosis (2,3). The precise pathophysiology of vascular calcification in ESRD is unknown, but risk factors include age, hypertension, time on dialysis, and, most significant, abnormalities in calcium (Ca) and phosphate (P) metabolism (4,5). Normal serum concentrations of Ca and inorganic P ions are metastable with respect to basic calcium phosphate (BCP; a mixture of octacalcium phosphate, dicalcium phosphate dihydrate, and apatite) precipitation but can support growth of nascent crystals. In ESRD, systemic Ca and inorganic P concentrations typically exceed 2.4 and 2.0 mM, respectively (4). Consequently, calcification in ESRD has traditionally been ascribed to supersaturation and subsequent precipitation of mineral ions. This has led to therapeutic measures to reduce the Ca/P product aimed mostly at reduction of P.Recent studies have shown that vascular calcification is a regulated process similar to bone formation (6,7). VSMC in the normal artery wall constitutively express potent inhibitors of calcification, such as matrix Gla ...

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Assay for Human Matrix Gla Protein in Serum

Cited by 82 publications

References 21 publications

Association of matrix γ-carboxyglutamic acid protein levels with insulin resistance and Lp(a) in diabetes: A cross-sectional study

Association of matrix γ-carboxyglutamic acid protein levels with insulin resistance and Lp(a) in diabetes: A cross-sectional study

Relationship Between Brachial Arterial Endothelial Function and Lumbar Spine Bone Mineral Density in Postmenopausal Women

Human Vascular Smooth Muscle Cells Undergo Vesicle-Mediated Calcification in Response to Changes in Extracellular Calcium and Phosphate Concentrations

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