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PubMed1984

Effects of suppression of eggshell calcification and of 1,25(OH)2D3 on Mg2+, Ca2+ and Mg2+HCO-3 ATPase, alkaline phosphatase, carbonic anhydrase and CaBP levels--II. The laying hen intestine.

Activity of a HCO-3 stimulated Mg2+ dependent ATPase is demonstrated in mitochondrial fractions of the avian duodenum. Suppression of eggshell calcification resulted in a slight reduction in Mg2+, Ca2+ and Mg2+HCO-3 ATPase activities. Duodenal carbonic anhydrase activity was lower in birds laying soft-shelled eggs than in birds laying normal eggs. Alkaline phosphatase and calcium binding protein levels both decreased along the length of the small intestine, but the effect was more pronounced for alkaline phosphatase. Suppression of eggshell calcification and treatment of shell-less laying hens with 1,25(OH)2D3 influenced alkaline phosphatase activity only in the duodenal mucosa. Suppression of eggshell calcification reduced CaBP levels in all sections of the intestine. Treatment with 1,25(OH)2D3 restored CaBP levels. Regulation of intestinal CaBP levels by 1,25(OH)2D3 would therefore, seem to be controlled more directly by calcium requirements associated with eggshell calcification than by gonadal hormones.

Adenosine Triphosphatases↗
PubMed1986

A possible role for polyamines in cartilage in the mechanism of calcification.

The role of polyamines in cartilage is not known: they may be somehow related to the mechanism of calcification. In epiphyseal cartilage from calf scapulas, they are more concentrated in the ossifying area, where calcification takes place, than in the resting region. Spermidine is present in greater amounts than spermine and putrescine. Since ornithine decarboxylase (EC 4.1.1.17) is measurable only in the resting region of the tissue, it is in this area that polyamine biosynthesis occurs, while they accumulate in the ossifying area. Immunohistochemical evidence is obtained that only in the ossifying zone is spermidine extracellular. It is at this level that the matrix is rearranged to become calcified, and proteoglycans are dissociated and partially removed. The effect of polyamines on solutions of proteoglycan subunits has been studied in vitro by following variations of turbidity and viscosity. While in the presence of putrescine the specific viscosity decreases to asymptotic values, in the presence of either 30 mM spermidine or 2.5-10 mM spermine, the decrement is more marked. At the same concentrations, increase of the turbidity of proteoglycan subunit solutions was observed. Only spermidine showed the capacity of displacing proteoglycan subunits from a column of Sepharose 4B-type II collagen: at 15 mM concentration, about 90% of proteoglycans were removed from the column. Alkaline phosphatase activity, which plays an important role in calcification, is enhanced by spermidine and spermine. These results obtained in vitro support the hypothesis that polyamines may be related to calcification of preosseous cartilage.

Alkaline Phosphatase↗
PubMed1991

Induction of metallothionein and stimulation of calcification by dexamethasone in cultured clonal osteogenic cells, MC3T3-E1.

To clarify the effects of dexamethasone (Dex) on metallothionein (MT) synthesis and calcification in osteoblastic cells, a clonal osteogenic cell line (MC3T3-E1) was used in the present study. Under culture conditions designed not to cause calcification, MT synthesis of cells at 3 days after inoculation increased with increasing concentration of Dex (2.5-50 nM) for a 24-h culture period. Cells at 6 or 9 days after inoculation also synthesized MT by a 24-h exposure to Dex. These show that undifferentiated osteoblasts have the ability to synthesize MT by Dex. Under culture conditions designed to cause calcification, cells at 6 days after inoculation were cultured with 50 nM Dex in the presence of 7 mM beta-glycerophosphate (beta-GP) for 7 days. Ca content of Dex-treated cells was about 7.5 times as high as that of untreated cells. Dex-treated cells showed a high activity of alkaline phosphatase (ALP). The Zn content of the MT fraction in Dex-treated cells was about 8 times as high as that of untreated cells. These results show that Dex has the ability to induce MT synthesis in osteoblastic cells and to cause a high calcification which is due at least partly to an enhanced activity of ALP.

Alkaline Phosphatase↗
PubMed2003

Basic calcium phosphate crystals stimulate the endocytotic activity of cells--inhibition by anti-calcification agents.

Pathological calcifications are associated with many medical conditions including diabetes, breast cancer, and crystals-associated osteoarthritis. The deposition of calcium-containing crystals on cells induces detrimental cellular effects and speeds up the progression of associated diseases. We carried out the present study to test the hypotheses that calcium-containing crystals may stimulate the influx of other molecules existing in the extracellular fluid disturbing normal molecular signaling and that anti-calcification agent will inhibit such endocytotic process. We found that basic calcium phosphate (BCP) crystals greatly stimulated the endocytotic activity of cells by rendering the cells more permeable and that the anti-calcification agent phosphocitrate and several others inhibited the crystals-mediated endocytosis. This is the first study reporting that the endocytotic activity of cells is affected by BCP crystals and that such endocytotic activity can be inhibited by anti-calcification agents. Since calcium-containing crystals are associated with many human diseases and in many circumstances are associated with apoptotic bodies, extracellular and matrix vesicles where DNA fragments, small peptides, and minerals are released into extracellular space, the findings reported here are important for our understanding of the complex biological effects and the potential pathological role of calcium-containing crystals in crystals-associated diseases, and for the development of disease modifying agents as well.

Breast Neoplasms↗
PubMed2005

Analysis of coronary calcifications versus Framingham and PROCAM risk assessment in patients with a first myocardial infarction.

UNLABELLED: We compared the extent of coronary calcifications as quantified by electron beam tomography (EBT) to the predicted 10-year cardiovascular event risk based on Framingham and PROCAM algorithms in patients with a first myocardial infarction (MI). METHODS: In 156 patients (56.7 +/- 22 years), EBT was performed <4 weeks after MI. Coronary calcifications were quantified using the "Agatston Score" and age-related calcium percentiles were determined. The predicted 10-year event risk was determined using Framingham and PROCAM algorithms. RESULTS: Coronary calcifications were present in 148 patients with a mean "Agatston Score" of 589.2 +/- 976. The "Agatston Score" was >400 in 44% and >90th percentile in 42% of the patients. Framingham risk was >20% in 32% and PROCAM risk was >20% in 28%. CONCLUSION: Coronary calcifications were detected in the vast majority of patients with a first MI, independent from the patient's age. The determination of age-related percentiles was superior to the Framingham or PROCAM algorithm.

Adult↗
PubMed2003

Physiological regulation of carbon fixation in the photosynthesis and calcification of coccolithophorids.

Emiliania huxleyi and Gephyrocapsa oceanica are the predominant coccolithophorid species that produce blooms in the ocean and affect the global environment. These species are capable of carbon fixation by both photosynthesis for organic matter production and by intracellular calcification for coccolith production. Both processes were strongly affected by the nutrient status in a laboratory culture. The coccolith production was stimulated by the addition of a high concentration of sodium bicarbonate and by the depletion of phosphate. Interestingly, when the calcification was stimulated, the increase in cell number during algal growth was greatly suppressed and then the cell volume increased. When the growth rate was increased under nutrient-sufficient conditions, the cells became very small in size and most of them bore few or no coccoliths. The data from laboratory experiments show that the cell growth and calcification proceeded apparently independently at different phases. We, therefore, assume that the coccolithophorid blooms in the ocean might be separated into two phases; firstly, the increase in cell population might be triggered by an adequate supply of nutrients to enhance algal growth and then the calcification might subsequently be stimulated when the nutrients become depleted by substantial algal growth.

Calcification, Physiologic↗
PubMed2002

Tocotrienols are needed for normal bone calcification in growing female rats.

In this study the effects of vitamin E deficiency and supplementation on bone calcification were determined using 4-month-old female Sprague-Dawley rats. The rats weighed between 180 and 200 g. The study was divided in three parts. In experiment I the rats were given normal rat chow (RC, control group), a vitamin E deficient (VED) diet or a 50% vitamin E deficient (50%VED) diet. In experiment 2 the rats were given VED supplemented with 30 mg/kg palm vitamin E (PVE30), 60 mg/kg palm vitamin E (PVE60) or 30 mg/kg pure alpha-tocopherol (ATF). In experiment 3 the rats were fed RC and given the same supplements as in experiment 2. The treatment lasted 8 months. Vitamin E derived from palm oil contained a mixture of ATF and tocotrienols. Rats on the VED and 50%VED diets had lower bone calcium content in the left femur compared to the RC group (91.6 +/- 13.3 mg and 118.3 +/- 26.0 mg cf 165.7 +/- 15.2 mg; P < 0.05) and L5 vertebra (28.3 +/- 4.0 mg and 39.5 +/- 6.2 mg compared with 51.4 +/- 5.8 mg; P < 0.05). Supplementing the VED group with PVE60 improved bone calcification in the left femur (133.6 +/- 5.0 mg compared with 91.6 +/- 13.3 mg; P < 0.05) and L5 vertebra (41.3 +/- 3.3 mg compared with 28.3 +/- 4.0 mg; P < 0.05) while supplementation with PVE30 improved bone calcium content in the L5 vertebra (35.6 +/- 3.1 mg compared with 28.3 +/- 4.0 mg; P < 0.05). However, supplementation with ATF did not change the lumbar and femoral bone calcium content compared to the VED group. Supplementing the RC group with PVE30, PVE60 or ATF did not cause any significant changes in bone calcium content. In conclusion, vitamin E deficiency impaired bone calcification. Supplementation with the higher dose of palm vitamin E improved bone calcium content, but supplementation with pure ATF alone did not. This effect may be attributed to the tocotrienol content of palm vitamin E. Therefore, tocotrienols play an important role in bone calcification.

Animals↗
PubMed1996

Evidence of the presence of a specific ATPase responsible for ATP-initiated calcification by matrix vesicles isolated from cartilage and bone.

Accumulating evidence indicates that calcification by isolated mammalian matrix vesicles (MVs) can be initiated by ATP. Since ATP can be hydrolyzed by either a specific ATPase or by nonspecific alkaline phosphatase (ALP), it remains to be established whether ATPase or ALP mediates ATP-initiated Ca and Pi deposition. To support the hypothesis that specific ATPase is responsible for ATP-initiated calcification by MVs isolated from mammalian cartilage and bone, the effects of ATP analogs, ALP substrates, and specific inhibitors on ATP hydrolysis and ATP-initiated calcification were compared between intact MVs and monoclonal antibody affinity-purified MV ALP. ATP analogs such as ADP and AMP exerted marked inhibitory effects on both [gamma-32P]ATP hydrolysis and ATP-initiated calcification by intact MVs, whereas phosphomonoesters such as beta-glycerophosphate or phosphoethanolamine had no effect. In contrast to intact MVs, purified MV ALP failed to calcify, and its [gamma-32P]ATP hydrolytic activity was readily inhibited by phosphomonoesters. Additionally, [gamma-32P]ATP hydrolysis by purified ALP in contrast to that by intact vesicles was completely inhibited by l-tetramisole, a specific inhibitor of ALP, suggesting a loss of specific ATPase during purification. Vanadate inhibition of ATP hydrolysis by purified ALP can be decreased by increasing ATP concentrations. On the contrary, ATP concentrations did not affect vanadate inhibition of ATP hydrolysis by intact MVs if ALP activity was blocked by l-tetramisole. These observations, therefore, suggest that: 1) a portion of [gamma-32P]ATP hydrolysis by MVs is attributable to a specific ATPase, whereas the remaining activity is due to ALP; and 2) a specific ATPase, but not ALP, is responsible for ATP-dependent Ca- and Pi-depositing activity of MVs isolated from bone or cartilage.

Adenosine Monophosphate↗
PubMed2005

Dyslipidemia and progression of cardiovascular calcification (CVC) in patients with end-stage renal disease (ESRD).

Dyslipidemia and progression of cardiovascular calcification (CVC) in patients with end-stage renal disease (ESRD). Cardiovascular calcification (CVC) is commonly encountered both in the general population as well as in patients with end-stage renal disease (ESRD). The etiology of CVC in patients with ESRD is multifactorial. Despite that, current debate remains narrowly focused on the role of calcium loading from calcium-based phosphate binders (CBPB) in the pathogenesis and progression of CVC. Yet, the alleged link between these binders and CVC has not been substantiated in well-designed controlled trials. In contrast, the purported role of sevelamer, a non-calcium-based phosphate binder, in slowing the progression of CVC in dialysis patients has attracted widespread attention. The beneficial effect of sevelamer on progression of calcification was thought to be due to lower calcium loading during its use. However, an alternative and possibly more likely mechanism involves sevelamer-induced lowering of LDL cholesterol. In this context, previous studies in individuals with normal renal function have documented amelioration of coronary artery calcification (CAC) with reduction of LDL-cholesterol by treatment with HMG-CoA reductase inhibitors (statins). Given that CAC is a well-accepted marker of atherosclerosis, and that high plasma cholesterol concentration is one of the main risk factors for atherosclerosis, then it is not unreasonable to suspect that CAC may be halted or even reversed by lowering of LDL cholesterol level with statin therapy. Unfortunately, the effect of lowering the LDL-cholesterol level on CAC has not been studied in patients with ESRD. Therefore, conclusions about this important topic should await the results of well-designed clinical studies that control for all factors potentially implicated in the CVC burden of patients with ESRD. In this review, I will discuss the role of various potential mechanisms involved in the pathogenesis of CVC in patients with ESRD, and emphasize the role of dyslipidemia and its treatment in this important clinical entity.

Calcification, Physiologic↗
PubMed1992

Calcification in human osteoblasts cultured in medium conditioned by the prostatic cancer cell line PC-3 and prostatic acid phosphatase.

A medium that had been conditioned by PC-3 cells stimulated the calcification of a human osteoblastic cell line, Tak-10, in a nonmitogenic culture. The calcification of the osteoblasts was stimulated maximally at a 25% concentration of the conditioned medium. Calcification activity was markedly enhanced by the addition of both prostatic acid phosphatase (PAP) and its substrate, alpha-glycerophosphate, to the medium; however, PAP added alone did not enhance this activity. These results suggest that human prostatic carcinoma cells produce a factor that stimulates the calcification of the human osteoblasts. Results have also suggested that PAP is a requisite for osteogenesis provided that its substrates are abundant in the medium.

Acid Phosphatase↗
PubMed2000

Phosphate regulation of vascular smooth muscle cell calcification.

Vascular calcification is a common finding in atherosclerosis and a serious problem in diabetic and uremic patients. Because of the correlation of hyperphosphatemia and vascular calcification, the ability of extracellular inorganic phosphate levels to regulate human aortic smooth muscle cell (HSMC) culture mineralization in vitro was examined. HSMCs cultured in media containing normal physiological levels of inorganic phosphate (1.4 mmol/L) did not mineralize. In contrast, HSMCs cultured in media containing phosphate levels comparable to those seen in hyperphosphatemic individuals (>1.4 mmol/L) showed dose-dependent increases in mineral deposition. Mechanistic studies revealed that elevated phosphate treatment of HSMCs also enhanced the expression of the osteoblastic differentiation markers osteocalcin and Cbfa-1. The effects of elevated phosphate on HSMCs were mediated by a sodium-dependent phosphate cotransporter (NPC), as indicated by the ability of the specific NPC inhibitor phosphonoformic acid, to dose dependently inhibit phosphate-induced calcium deposition as well as osteocalcin and Cbfa-1 gene expression. With the use of polymerase chain reaction and Northern blot analyses, the NPC in HSMCs was identified as Pit-1 (Glvr-1), a member of the novel type III NPCs. These data suggest that elevated phosphate may directly stimulate HSMCs to undergo phenotypic changes that predispose to calcification and offer a novel explanation of the phenomenon of vascular calcification under hyperphosphatemic conditions. The full text of this article is available at http://www.circresaha.org.

Arteries↗
PubMed1993

Calcification of chick vertebral chondrocytes grown in agarose gels: a biochemical and ultrastructural study.

Chick embryo vertebral chondrocytes (CHECOV cells) grown in agarose gels form spherical colonies containing cells of hypertrophic morphology and a metachromatically staining matrix. Biochemical analysis of these cultures resulted in the following findings. (i) Calcification of CHECOV cultures can be induced by addition of Pi (at least 1.9 mM) or beta-glycerol phosphate (BGP). (ii) Alkaline phosphatase activity reaches a maximal value at the time when mineral deposition is initiated. (iii) Added BGP is converted to Pi; maximal production of Pi occurs at the time of maximal alkaline phosphatase activity. (iv) BGP-supplemented cultures produce a degree of calcification that corresponds to the amount of BGP conversion to Pi. It can be concluded that Pi is rate-limiting for the calcification of chondrocyte cultures. BGP promotes calcification of these cultures by acting as a substrate for the alkaline phosphatase-mediated production of inorganic phosphate.

Alkaline Phosphatase↗
PubMed1986

The calcium antagonist diltiazem inhibits calcification enhanced by calcitonin in growth cartilage of rats in ethane-1-hydroxy-1,1-diphosphonate (EHDP)-induced rickets.

In an animal model of human rickets developed by giving a short-term administration of large doses of EHDP to young rats, concomitant administration of [Asu1,7]eel calcitonin (CT) with EHDP resulted in the promotion of calcification in growth cartilage. In an attempt to clarify the mechanisms related to the accelerated calcification due to CT, the effects of diltiazem, a calcium antagonist, were studied. Diltiazem suppressed, in a dose-dependent manner, the accelerated calcification due to CT in the growth cartilage, as determined by findings on the soft X-ray photos, contact microradiograph and light microscopic histology of the proximal region of the tibia. This suppression was only evident when diltiazem and CT were given concomitantly. If it is assumed that diltiazem inhibits the entry of calcium ion into the cells of growth cartilage, in the same manner as seen in case of smooth muscle and myocardial cells, then our results indicate that intracellular concentrations of calcium might play an important role in the occurrence of accelerated calcification due to CT.

Animals↗
PubMed1975

Calcification of rachitic rat cartilage in vitro by extracellular matrix vesicles.

Growth plate cartilage from rachitic rats was studied to assess the role in calcification of extracellular matrix vesicles, which are thought to participate in the initial stage of mineralization of connective tissue. The concentration of matrix vesicles and their distribution within the longitudinal septa was found to be normal in rats made rachitic by feeding by a diet low in vitamin D and phosphate for 3 weeks after weaning. Rachitic cartilage matrix did not contain circumvesicular clusters of apatite as does normal cartilage; however, occasional vesicles did enclose one or a few apatite needles. When slices of rachitic cartilage were incubated at 37 C in a metastable calcium phosphate solution ([Ca++] times [PO SEE ARTICLE] equals 3.5 mM identical to 2), apatite formation was initiated in association with matrix vesicles. Under these conditions, mineralization was prominent in the upper hypertrophic cartilage, where matrix vesicles became encrusted with apatite after only 2 to 3 hours of incubation. Vesicular apatite accumulation was inhibited by preheating the cartilage to 60 C for 30 minutes. Measurements of 45Ca uptake by rachitic cartilage slices from metastable calcium phosphates solution also indicated inhibition of calcification by heat. Light microscopic autoradiographs showed 45Ca localization primarily in the matrix of longitudinal septa and substantiated the inhibition site of mineralization in healing rachitic cartilage. The presence of apatite within rachitic vesicles prior to heating and the inhibition of vesicle calcification by heat suggests an active, enzymatically and mediated mechanism of vesicular calcification.

Animals↗
PubMed2001

Ultrastructural analysis of bone calcification by using energy-filtering transmission electron microscopy.

In order to elucidate the mechanisms of bone calcification, embryonic rat calvariae treated with chemical or cryo-fixation were observed using transmission electron microscopy by three techniques: fine structures, various cvtochemical localizations including nonspecific proteoglycan, decorin, chondroitin 4-sulfate, hyaluronan, alkaline phosphatase (ALP), and osteonectin, as well as the elemental mapping of calcium and phosphorus by energy-filtering electron microscopy. In the calvariae, the calcification sequence ran as follows crystallization within matrix vesicles, formation of calcified nodules, collagen calcification, and finally the establishment of an expansive calcified matrix. The osteoid contained an abundance of mesh-like fibers of proteoglycans, including decorin, chondroitin 4-sulfate, and hyaluronan, around collagen fibrils approximately 50 nm in diameter. Calcium tended to localize at the proteoglycan sites, while phosphorus was often mapped to the collagen fibril-structures in the osteoid. Calcium/phosphorus co-localization was found in and around the calcified nodules, where ALP and small sized proteoglycans were observed. During this stage, native proteoglycans surrounding the collagen fibrils disappeared, with the collagen fibrils fusing laterally, and attaining a diameter of more than 400nm. The calcified nodules expanded to occupy the entire space made available by the collagen fibril-fusion, following osteonectin accumulation in the calcified nodule/collagen fibril border. In conclusion, crystals present within the matrix vesicles became calcified nodules, in a process induced by the co-localization of calcium and phosphorus. ALP and proteoglycans may participate in the calcium/phosphorus co-localization. Decreases in the native proteoglycans, and the lateral fusion of collagen fibrils are thought to be involved in the expansion of calcified areas, followed by osteonectin-mediated collagen calcification.

Alkaline Phosphatase↗
PubMed2004

[Control of calcification by extracellular matrix].

Physiological calcification begins from crystallization of hydroxyapatite in extracellular matrix of both bones and teeth. Because calcification is exactly the extracellular event, organic components of extracellular matrix play important roles in control of calcification. The authors discuss the molecular regulation of calcification by organic components of extracellular matrix, focusing on the mineral/organic interaction.

1-Carboxyglutamic Acid↗
PubMed2004

[Effects of traditional chinese medicine Drynaria fortunei smith on promoting the proliferation, differentiation and calcification of mouse osteoblastic MC3T3-E1 cells].

OBJECTIVE: To explore the effects of Drynaria fortunei J. Smith (DFS) on promoting the proliferation, differentiation and calcification of cells. METHOD: Two DFS preparations were extracted with distilled water (DFS aqueous-extract) and 95% ethanol (DFS ethanol-extract), respectively. A mouse osteoblast cell line MC3T3-E1 was used as a cell model for screening potency of DFS. MTT and Flow cytometry were applied to determine proliferation of the cell promoted by DFS aqueous-and ethanol-extracts at different dosages. Differentiating effects of the two extracts with different concentrations in the cell were evaluated through the examinations of alkali phosphate (ALP) activities and osteocalcin levels. Von kossa staining method was used to understand the effects of the two extracts promoting calcification of the cell. RESULT: 0.01 mg x L(-1) and 1 mg x L(-1) of DFS aqueous-extracts showed the proliferative promotion for MC3T3-E1 cell (P < 0.05). Both the 0.01 mg x L(-1) and 1 mg x L(-1) of the two DFS extracts increased the percentages of S-phase cells whereas the percentages of G1-phase cells were decreased. 1 and 100 mg x L(-1) of the ethanol-extract remarkably increased the synthesis and secretion of osteocalcin of the cell (P < 0.001). 1 mg x L(-1) of the aqueous-extract and 0.01 mg x L(-1) of the ethanol-extract were able to promote the cell calcification (P < 0.05). CONCLUSION: In the DFS aqueous-and ethanol-extracts, there are some of the components promoting the proliferation, differentiation and calcification of osteoblast.

Animals↗
PubMed1991

Role of proteoglycan in the provisional calcification of cartilage. A review and reinterpretation.

Study of the calcification of cartilage in endochondral ossification has yielded two apparently contradictory views of the role of proteoglycan in this process. The ability of proteoglycan to act as a calcium-concentrating agent (Kalksalzfänger) in cartilage is consistent with the view that proteoglycans are promoters of calcification. However, study of their effect on hydroxyapatite formation in vitro suggests that proteoglycans are inhibitors of cartilage calcification. A resolution of this paradox is now proposed. Proteoglycans inhibit hydroxyapatite formation under in vitro conditions of limited calcium availability (in part) by binding calcium ions. However, under in vivo conditions of essentially infinite calcium availability, proteoglycans may promote hydroxyapatite formation, since binding of calcium to proteoglycan will not decrease the free calcium concentration, and the bound calcium may easily be displaced. Therefore, it is proposed that the role of proteoglycans in the calcification of cartilage is to function as a cation-exchanging calcium reservoir.

Animals↗