Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Matrix Gla Protein”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 325 records · Page 18Linked to original sources
PubMed2003

Characterization of gene expression profiles associated with glioma progression using oligonucleotide-based microarray analysis and real-time reverse transcription-polymerase chain reaction.

Diffuse astrocytoma of World Health Organization (WHO) grade II has an inherent tendency to spontaneously progress to anaplastic astrocytoma (WHO grade III) and/or glioblastoma (WHO grade IV). The molecular basis of astrocytoma progression is still poorly understood, in particular with respect to the progression-associated changes at the mRNA level. Therefore, we compared the transcriptional profile of approximately 6800 genes in primary WHO grade II gliomas and corresponding recurrent high-grade (WHO grade III or IV) gliomas from eight patients using oligonucleotide-based microarray analysis. We identified 66 genes whose mRNA levels differed significantly (P < 0.01, > or =2-fold change) between the primary and recurrent tumors. The microarray data were corroborated by real-time reverse transcription-polymerase chain reaction analysis of 12 selected genes, including 7 genes with increased expression and 5 genes with reduced expression on progression. In addition, the expression of these 12 genes was determined in an independent series of 43 astrocytic gliomas (9 diffuse astrocytomas, 10 anaplastic astrocytomas, 17 primary, and 7 secondary glioblastomas). These analyses confirmed that the transcript levels of nine of the selected genes (COL4A2, FOXM1, MGP, TOP2A, CENPF, IGFBP4, VEGFA, ADD3, and CAMK2G) differed significantly in WHO grade II astrocytomas as compared to anaplastic astrocytomas and/or glioblastomas. Thus, we identified and validated a set of interesting candidate genes whose differential expression likely plays a role in astrocytoma progression.

Adult↗
PubMed2005

Anabolic actions of PTH (1-34): use of a novel tissue engineering model to investigate temporal effects on bone.

PTH is in clinical use for the treatment of osteoporosis and is under intensive investigation for its potential in applications of tissue engineering, fracture healing, and implant integration. However, the mechanisms of its action to stimulate bone formation are still unclear. A novel bone tissue engineering model was used to elucidate basic mechanisms of PTH anabolic actions. Ectopic ossicles containing cortical bone, trabecular bone, and a hematopoietic marrow were generated from implanted bone marrow stromal cells (BMSC). One week after implantation, nude mice were administered PTH or vehicle for 1 week (group 1), 3 weeks (group 2), or 7 weeks (group 3). Another group was also treated for 3 weeks, initiated 12 weeks after implantation (group 4). Micro-radiography and histomorphometry revealed increased marrow cellularity in group 1 PTH-treated ossicles, increased bone in group 2 PTH-treated ossicles, and similar amounts of bone in both group 3 and 4 ossicles regardless of treatment. Incidence of phosphate mineral and phosphate mineral to hydroxyproline ratio via Raman spectroscopy were significantly higher after 3 weeks versus 1 week of PTH treatment, but there was no difference between PTH- and vehicle-treated ossicles. Early events of PTH action in group 1 ossicles and the effects of a single injection of PTH on 1- and 2-week-old ossicles were evaluated by Northern blot analysis. Osteocalcin (OC) mRNA was increased after 1 week of intermittent PTH treatment in ossicles and calvaria but an acute injection did not alter OC mRNA. In contrast, a single injection of PTH increased matrix gamma-carboxyglutamic acid protein (MGP) mRNA in 2-week-old ossicles. Differential and temporal-dependent effects of PTH on OC and MGP suggest at the molecular level, that PTH acts to inhibit osteoblast mineralization. However, this does not translate into tissue level alterations. These data indicate that anabolic actions of PTH in ectopic ossicles are temporally dependent on the BMSC implanted and suggest that cell implantation strategies are particularly responsive to PTH.

Adipocytes↗
PubMed2002

Novel effects of diets enriched with corn oil or with an olive oil/sunflower oil mixture on vitamin K metabolism and vitamin K-dependent proteins in young men.

Little is known of how the fat components of diets influence the absorption and metabolism of vitamin K and the possible consequences to the synthesis of vitamin K-dependent (VKD) proteins in different target organs. We have evaluated the effects of two diets on circulating phylloquinone (K1) and triacylglycerols (TAG). One diet was enriched with corn oil (CO) (also rich in gamma-tocopherol) and the other with an olive/sunflower (O/SO) mixture (rich in alpha-tocopherol). Effects on gamma-carboxylation were assessed from coagulation assays and sensitive assays for undercarboxylated prothrombin (ucFII) and osteocalcin (ucOC). Total plasma matrix Gla-protein (MGP) was also measured. After an initial adjustment diet, 26 healthy young men were fed, in a crossover design, the O/SO or CO diet for 2 weeks. Mean intakes of K1 during consumption of adjustment, O/SO, and CO diets were 225 microg/day, 291 microg/day, and 291 microg/day, respectively. Mean fasting levels of TAG and K1 were both significantly reduced by the CO diet, but not by the O/SO diet. Neither diet reduced FII activity but ucFII became detectable in nine subjects, eight of whom showed this abnormality with both diets. The CO diet induced a rise in ucOC (P < 0.05), which was negatively correlated to ucFII (r = -0.71, P < 0.03). The CO but not O/SO diet induced a decrease of total circulating MGP. We conclude that both oils, notably CO, affected vitamin K absorption and/or metabolism which may increase the requirements for gamma-carboxylation. The mechanism is unclear but may result from interactions of vitamin K with PUFA and/or other lipid components such as vitamin E.

Adult↗
PubMed2001

Vitamin D control of osteoblast function and bone extracellular matrix mineralization.

Vitamin D is the major regulator of calcium homeostasis and protects the organism from calcium deficiency via effects on the intestine, kidney, parathyroid gland, and bone. Disturbances in the vitamin D endocrine system (e.g., vitamin D-dependent rickets type I and type II), result in profound effects on the mineralization of bone. Recent studies with vitamin D receptor knockout mice also show effects on bone. It is questioned whether vitamin D has a direct effect on bone formation and mineralization. In rickets and particular vitamin D receptor knockout mice, calcium supplementation restores bone mineralization. However, the vitamin D receptor is present in osteoblasts, and vitamin D affects the expression of various genes in osteoblasts. This review focuses on the role of vitamin D in the control of osteoblast function and discusses the current knowledge of the direct effects of vitamin D on mineralization. Moreover, the role of vitamin D metabolism and the mechanism of action of vitamin D and interaction with other hormones and factors are discussed.

Alkaline Phosphatase↗
PubMed1989

Dentin matrix proteins: composition and possible functions in calcification.

Dentin may be regarded as a mineralized connective tissue. In its composition as well as its mode of formation, dentin exhibits several similarities with bone, but also definite differences. The dentin organic phase, the matrix, determines its morphology and is believed to be instrumental in the formation of the mineral phase. A fibrous web of collagen type I dominates the organic matrix. Also, minor amounts of other collagen types may be present. The noncollagenous proteins (NCPs), which constitute about 10% of the matrix, fall into several categories: phosphoproteins, Gla-proteins of the osteocalcin type as well as matrix Gla-protein, proteoglycans, different acidic glycoproteins, and serum proteins. Some of these NCPs have unique chemical compositions that give them specific properties. Dentinogenesis occurs by two simultaneous processes: the formation of a collagenous web in predentin, which is followed by the formation of the inorganic phase at the mineralization front. The composition of the predentin organic matrix differs from that of dentin, as some NCP components are secreted extracellularly just in advance of the mineralization front. In addition, some constituents of predentin seem to be metabolized. The NCPs may be important to several processes during dentinogenesis. Much evidence indicates that noncollagenous components in the matrix are instrumental in mineral formation. New data show that polyanionic NCPs, such as phosphoprotein and proteoglycans, when immobilized on a solid support, induce apatite formation under physiological conditions. These data indicate that polyanionic NCPs may function as mineral nucleators in vivo. They may also act as size and rate regulators for crystallization and promote calcium ion diffusion in the tissue. In addition, NCPs may regulate collagen fibrillogenesis.

1-Carboxyglutamic Acid↗
PubMed2001

Insights into the mechanism of vascular calcification.

Vascular calcification is common and clinically significant in atherosclerosis and heart failure. It was long believed to be an end-stage process of "passive" mineral precipitation. However, there is now a growing awareness that vascular calcification is a biologically regulated phenomenon. It has many similarities to bone formation, and ectopic bone is a well-documented part of vascular calcification. This implies that alterations in vascular cell differentiation, extensive or localized, are an integral part of vascular calcification. Matrix gamma-carboxylated glutamate (GLA) protein (MGP)-deficient mice develop extensive vascular calcification with replacement of the media by progressively calcifying cartilage. A potential mechanism that explains these findings is MGP interference with bone morphogenetic proteins-potent inducers of cartilage and bone.

Animals↗
PubMed2005

Warfarin therapy and systolic hypertension in men with atrial fibrillation.

BACKGROUND: Warfarin decreases the activity of matrix Gla-protein and causes extensive arterial calcification leading to increased systolic blood pressure (SBP) and pulse pressure (PP) in rats. We performed post hoc analyses of the Stroke Prevention in Non-Rheumatic Atrial Fibrillation (SPINAF) trial, aiming to analyze the effects of warfarin on SBP and PP. METHODS: The SPINAF trial was a randomized, double-blind, placebo-controlled trial comparing warfarin and placebo in 525 subjects with nonrheumatic atrial fibrillation. After exclusions for inadequate follow-up, 284 subjects with average treatment lasting 23.7 months were available for analysis (144 given placebo and 140 warfarin). RESULTS: Baseline SBP, diastolic blood pressure (DBP), mean arterial pressure (MAP), and PP were 132 +/- 18, 81 +/- 9, 98 +/- 11, and 50 +/- 16 mm Hg in the warfarin group, and 133 +/- 21, 80 +/- 13, 97 +/- 14, and 54 +/- 15 mm Hg in the placebo groups (all P values, NS). There was no statistically significant difference between the placebo and warfarin groups in any of the BP parameters at any time point. However, stratified analyses showed a significant increase in PP in warfarin-treated subjects with a history of hypertension (4.9 +/- 13.1 mm Hg v 0.2 +/- 11.9 mm Hg in the placebo group, P = 0.022), and those with baseline SBP > or =140 mm Hg (4.8 +/- 18.9 mm Hg v -3.4 +/- 11.2 mm Hg in the placebo group, P = .038). A similar trend was noted in diabetic subjects but it was not statistically significant. CONCLUSIONS: Based on the study results, treatment with warfarin does not result in increased BP in men with atrial fibrillation. However, it is possible that subjects at higher baseline cardiovascular risk may be more susceptible to the chronic effects of warfarin on arterial hemodynamics.

Aged↗
PubMed1988

The effects of short-term, high-dose treatment with prednisone on the nuclear uptake of 1,25-dihydroxyvitamin D3 in monocytes from normal human subjects.

Animal and cell culture studies indicate glucocorticoid regulation of 1,25-dihydroxyvitamin D3 receptors and interference with cellular effects of vitamin D. These investigations prompted us to examine the effects of prednisone on the nuclear uptake of 1,25-dihydroxyvitamin D3 in freshly isolated human monocytes. Eighteen normal subjects were studied in a randomized, double-blind, placebo-controlled study. Analysis of receptor kinetics revealed that the maximal nuclear uptake (Bmax) of (3H)-1,25-dihydroxyvitamin D3 in monocytes decreased 40% (P less than .001) after prednisone treatment. In the group treated with prednisone (40 mg/d for 5 days) s-1,25-dihydroxyvitamin D increased 46% (P less than .01). S-25-Hydroxyvitamin D, S-phosphat, S-calcium, and S-iPTH remained unchanged. Osteoblastic production of the matrix protein, bone gla protein (BGP) is stimulated by 1,25-dihydroxyvitamin D3. However, despite increased serum levels of 1,25-dihydroxyvitamin D3, the prednisone-treated group revealed a 75% reduction in s-BGP. The present data indicate that corticosteroids decrease the nuclear uptake of 1,25-dihydroxyvitamin D3 in human monocytes. Further investigations are necessary, however, to elucidate the biologic mechanism for this observation and whether the mechanism is operative in other human tissues including bone.

Adult↗
PubMed2005

Vitamin K1 intake and coronary calcification.

OBJECTIVES: The activity of matrix Gla-protein (MGP), a potent inhibitor of vascular calcification, is dependent on carboxylation using vitamin K as a co-factor. In animals, low intake of total vitamin K has been shown to accelerate vascular calcification via the MGP mechanism. This has led to the hypothesis that low levels of dietary vitamin K intake may be a risk factor for accelerated vascular calcification in humans due to decreased MGP activity. Additionally, some authors have suggested that current recommended daily intake values for vitamin K might be insufficient to fully inhibit vascular calcification via the MGP mechanism. The aim of this study was to examine the relationship between dietary vitamin K1 (the most prevalent dietary form of vitamin K) intake and premature coronary artery calcification (CAC) in an asymptomatic screening population. METHODS: We conducted a prospective study of 807 consecutive active-duty US Army personnel, 39-45 years of age, without known coronary heart disease. Vitamin K1 intake was measured with the Block Dietary Questionnaire and CAC was identified using electron-beam computed tomography (EBCT). RESULTS: We found no significant correlation between CAC score and vitamin K1 intake (r = 0.132, P = 0.106). Multivariate analysis with adjustment for cardiac risk factors showed no association between dietary vitamin K1 intake and CAC. CONCLUSIONS: Dietary vitamin K1 (phylloquinone) intake appears to be unrelated to premature coronary calcification in a screening population. Further investigation into the relationship of vascular calcification and other forms of vitamin K1 (menaquinones) is indicated.

Adult↗
PubMedDate not supplied

[Prevention of extraskeletal calcifications in uremia].

Secondary hyperparathyroidism (HPTH) is a common feature in end-stage renal disease (ESRD) patients. The three main factors involved in secondary HPTH pathogenesis are high phosphate levels, hypocalcemia and vitamin D deficiency. Recently, many studies demonstrated a strong association between bone disease and cardiovascular events in chronic kidney disease patients. In addition, cardiovascular events are the most frequent cause of death in patients with chronic renal failure. Increased levels of serum phosphorus and calcium-phosphate product are directly involved in the pathogenesis of extraskeletal calcifications (blood vessels, soft tissues, etc) in dialyzed patients compared to the non-uremic population. Recent studies suggested that vascular calcification is due not only to a passive calcium-phosphate deposition on atherosclerotic arteries, but also to active mechanisms regulated by bone-associated genes. In particular, fetuin and matrix Gla-protein are two 'protective' proteins associated with reduced vascular calcification and could be the regulatory keys in preventing this process in renal failure. The limitations of calcium salts as phosphate-binders in patients with advanced renal failure have been thoroughly evaluated in the last 5 yrs. New phosphate binders, which do not contain aluminum or calcium, have been developed to reduce the risk of extraskeletal calcifications in ESRD.

Animals↗
PubMed1998

The role of Gla proteins in vascular calcification.

Arterial calcification occurs with increasing age and in association with a diverse range of diseases, including atherosclerosis, diabetes, and uremia. It occurs at two sites in the vessel wall--in the media where it is known as Monckeberg's sclerosis and in the intima where it is invariably associated with atherosclerosis. Although there are similarities between them, the molecular mechanisms underlying these two forms of calcification may be distinct. Evidence is accumulating that vascular calcification is an active process that has many similarities with ossification, including local expression of bone-associated collagenous and noncollagenous proteins. The recent generation of a matrix gamma-carboxyglutamic acid (Gla) protein (MGP) knockout mouse, which exhibits extensive and lethal calcification and cartilaginous metaplasia of the media of all elastic arteries, has refocused attention on the role of Gla-containing proteins in vascular calcification. Gla-containing proteins have glutamic acid residues that must by gamma-carboxylated by vitamin-K-dependent gamma-carboxylase to enable them to bind calcium and function normally. Therefore, there is considerable scope for both transcriptional and posttranslational modifications of Gla protein function. Recent studies in humans have shown that although MGP mRNA is constitutively expressed by normal vascular smooth muscle cells (VSMCs), it is substantially upregulated in cells adjacent to both medial and intimal calcification. Studies in rats and on cultured human VSMCs showing that inhibition of MGP function by warfarin can accelerate spontaneous calcification have emphasized the potential importance of posttranslational processing in determining MGP function. It is therefore plausible that environmental influences such as diet and medication may have significant effects on vascular calcification. Furthermore, recent studies have shown that several other Gla-containing proteins with the potential to regulate or perhaps contribute to vascular calcification are present in the human vasculature. Future studies on the role of Gla-containing proteins combined with advances in noninvasive imaging techniques to quantify vascular calcification may lead to identification of individuals at particular risk of vascular calcification and the evaluation of novel therapies aimed at regulating its development or progression.

1-Carboxyglutamic Acid↗
PubMed1992

Articular-cartilage matrix gamma-carboxyglutamic acid-containing protein. Characterization and immunolocalization.

Matrix gamma-carboxyglutamic acid (Gla)-containing protein (MGP) was found to be present in articular cartilage by Western-blot analysis of guanidinium chloride extracts of human and bovine cartilage and was further localized by immunohistochemical studies on human and monkey specimens. In newborn articular cartilage MGP was present diffusely throughout the matrix, whereas in growth-plate cartilage it was seen mainly in late hypertrophic and calcifying-zone chondrocytes. In adult articular cartilage MGP was present primarily in chondrocytes and the pericellular matrix. Immunoelectron microscopy studies revealed an association between MGP and vesicular structures with an appearance consistent with matrix vesicles. MGP may be an important regulator of cartilage calcification because of its localization in cartilage and the known affinity of Gla-containing proteins for Ca2+ and hydroxyapatite.

1-Carboxyglutamic Acid↗
PubMed1993

Adverse effects of coumarin anticoagulants.

The biochemistry of vitamin K metabolism and the role of vitamin K-dependent gamma-carboxylation of the vitamin K-dependent coagulation factors are now well understood. Likewise, there is a clear understanding of the role of oral anticoagulants in the inhibition of these coagulation factors. However, the effect of oral anticoagulants on extrahepatic gamma-carboxylated proteins such as osteocalcin and matrix gamma-carboxyglutamate (Gla)-protein (MGP), and the effects of long term anticoagulants on bone mineral metabolism are just now being recognised. The relevance of these observations on mineral metabolism for elderly individuals, and in particular postmenopausal women who are on long term anticoagulants, is still unknown but worthy of continued close observation. The most significant hazard of oral anticoagulants is haemorrhage. Clinical trials continue to demonstrate that less intense (lower dosage) warfarin therapy can significantly decrease this risk of haemorrhage while at the same time providing equal efficacy when compared to more intense warfarin therapy. The more widespread use of the International Normalised Ratio (INR) for the control of anticoagulants will undoubtedly further decrease the risk of haemorrhage, but new innovations such as the use of ultra low-dose warfarin or newer techniques for the continued monitoring of oral anticoagulants are still required, particularly as the indications for oral anticoagulants continue to expand.

Coumarins↗
PubMed2001

Expression and localization of MGP in rat tooth cementum.

Tooth cementum, a calcified hard tissue covering the root surfaces, is an important component connecting the teeth to the collagenous fibres of the periodontal ligament. Although the overall composition of cementum may closely resemble that of bone, each part has not been fully characterized. Here, the localization of the matrix gamma-carboxyglutamic acid (Gla) protein (MGP), one of the major Gla-containing proteins in the body, in cementum was investigated using immunohistochemistry and in situ hybridization. (1) Strong MGP antigenicity was observed in the acellular cementum, but was only moderate in the cellular cementum; (2) polygonal periodontal ligament cells facing the acellular cementum and the uncalcified cellular cementum expressed MGP mRNA, indicating that these cells produced MGP and deposited it on the cementum; (3) MGP accumulated at the junction between the uncalcified and calcified cellular cementum; and (4) the distribution pattern of MGP antigenicity resembled that of osteopontin. As one function of MGP could be as a negative regulator for mineral apposition, the expression of MGP in the cells adjacent to the cementum may be important to prevent hyperapposition of minerals.

Animals↗
PubMed1986

Effect of acute increases in bone matrix degradation on circulating levels of bone-Gla protein.

Serum bone Gla-protein (BGP), also called osteocalcin, is a specific and sensitive measure of bone turnover in a variety of metabolic bone disorders. Although some BGP diffuses into the circulation after synthesis by osteoblasts, most is incorporated into bone matrix where it remains until bone is resorbed. Thus, serum BGP could reflect bone formation, bone resorption, or a combination of both. The relationship of serum BGP to the components of bone turnover was evaluated in 18 normal women (mean age 48 yr; range 30-70) who received a continuous 24-h intravenous infusion of the 1-34 synthetic fragment of bovine parathyroid hormone. Mean +/- SE for urinary hydroxyproline excretion, an index of bone resorption, increased (from 22.7 +/- 2.2 to 38.5 +/- 3.7 micrograms/100 ml glomerular filtrate [GF], p less than .001), whereas levels of serum alkaline phosphatase, an index of bone formation, were unchanged (from 20 +/- 1 to 20 +/- 1 U/liter, NS). Despite the increase in bone resorption, levels of serum BGP decreased (from 8.8 +/- 0.8 to 6.8 ng/dl, p less than .001). The data suggest that circulating levels of BGP are a measure of bone formation but, at least in subjects with normal renal function, not a measure of bone resorption. Presumably BGP in bone matrix is degraded during osteoclastic resorption into fragments that either are not recognized by an antiserum raised against the native molecule or are rapidly cleared from the circulation.

Adult↗
PubMed1992

Protein-S, a vitamin K-dependent protein, is a bone matrix component synthesized and secreted by osteoblasts.

Protein-S is a vitamin K (Vit K)-dependent protein synthesized by hepatocytes, megakaryocytes, and endothelial cells and plays an important role in the regulation of hemostasis. Two cases of free protein-S congenital deficiency were recently reported to be associated with osteopenia. We hypothesized that this osteopenia could be the result of a bone deficit of protein-S synthesized by bone cells. Using enzyme-linked immunoassay, immunocytochemistry, immunoblotting, and immunoprecipitation after labeling with [35S]methionine, we have shown that this protein is secreted by three human osteosarcoma cell lines and by human adult osteoblast-like cells. In addition, protein-S was present in protein extracts of human bone matrix. Protein-S secreted by MG 63 cells increased linearly from 1-7 days of culture, was biologically active, and was regulated by warfarin, as previously described for the other cell types secreting protein-S. Vit K had no direct effect on protein-S secretion or activity, but could overcome the effects of warfarin. In conclusion, in addition to osteocalcin and matrix gamma-carboxyglutamic acid (Gla) protein, osteoblasts secrete another Vit K-dependent protein, which is a constituent of the bone matrix. Our data suggest that osteopenia occurring in patients with congenital protein-S deficiency might be related to a deficiency of protein-S secretion by the osteoblasts. This finding raises the intriguing possibility that protein-S might play a role in bone turnover and bone mass.

Bone Neoplasms↗
PubMed1997

Long-term oral anticoagulation reduces bone mass in patients with previous hemispheric infarction and nonrheumatic atrial fibrillation.

BACKGROUND AND PURPOSE: Vitamin K is an essential factor for synthesis of plasma clotting proteins and for site-specific carboxylation of bone Gla protein and other bone matrix proteins. Low vitamin K has been associated with reduced bone mineral density. Warfarin therapy, which inhibits vitamin K-dependent blood-clotting, has been demonstrated to reduce the risk of stroke in nonrheumatic atrial fibrillation. We evaluated vitamin K and bone mineral density in nonrheumatic atrial fibrillation patients who had long-term warfarin therapy after an ischemic stroke. METHODS: Sera were collected from 64 patients with non-rheumatic atrial fibrillation and ischemic stroke who had been treated with warfarin, 63 stroke patients without warfarin, and 39 control subjects. All stroke patients in both groups had hemiplegia. Sera were assayed for vitamins K1 and K2, bone Gla protein, and 25-hydroxyvitamin D. Bone mineral density was determined in both second metacarpals. RESULTS: Serum vitamin K1 concentrations (ng/mL) were lower in treated patients (.234 +/- .177 ng/mL) than in untreated patients (.329 +/- .284) or controls (.553 +/- .164). Bone Gla protein was lower in treated patients' sera (1.241 +/- .799 ng/mL) than in untreated patients (4.476 +/- 3.226). Concentrations of 25-hydroxyvitamin D were lower in both patient groups. Bone mineral density was lower on both sides in treated patients than in untreated patients (P < .0001). Vitamin K1 and bone Gla protein were significantly related to bone mineral density bilaterally in treated but not in untreated patients. CONCLUSIONS: Bone mineral density was significantly lower in stroke patients with long-term warfarin treatment than in untreated patients. Both warfarin-induced reduction in vitamin K function and lowered vitamin K1 concentrations are probable causes of this osteopenia.

Administration, Oral↗
PubMed1993

Detection and measurement of vitamins K1 and K2 in human cortical and trabecular bone.

Vitamin K plays an essential role in the gamma carboxylation of the gla-containing proteins of bone matrix, such as osteocalcin. We have measured the concentration of vitamin K1 (VK) and of the menaquinones MK-6, MK-7, and MK-8, the three major vitamin K2 moieties, in trabecular and cortical bone taken from the femoral neck of patients undergoing hip replacement. Both bone compartments were found to contain large amounts of VK, MK-6, MK-7, and MK-8. Concentrations were as high as those reported for the liver, the major storage organ for vitamin K. Further research is required to examine the association between vitamin K in bone and the gamma carboxylation of vitamin K-dependent bone proteins.

Aged↗