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At least 703 records · Page 39Linked to original sources
PubMed1979

An X-ray fluorescence technique for in vivo determination of lead concentration in a bone matrix.

We have previously reported the in vivo detection of lead in the skeleton of man by means of X-ray fluorescence analysis using a 740 MBq 57Co source for excitation and a 1 cm(3) Ge(Li) detector for registration of the Pb Kalpha and Kbeta radiation. The varying geometry, density and atomic composition of the tissues of interest (mainly fingers) introduce several problems in estimation of the true concentration of a given element. A two-component cylindrical finger phantom was therefore constructed from silica paraffin wax and animal bone ash. The diameter of the finger bone was estimated from X-ray examinations in two orthogonal projections. The bone mineral concentration was then estimated from the quotient of the number of coherent and Compton scattered primary photons. The lead concentration in the finger bones was then derived from a measurement on a finger phantom made of silica paraffin wax and bone ash with the same size and bone mineral concentration as the real bone. The minimum detectable lead concentration in a finger bone was 14 microgram g(-1) for 15 min measuring time. The lead concentration measured in workers from a metal industry was found to be in the range of 40-100 microgram g(-1).

Bone Matrix↗
PubMed1975

Demineralization of bone matrix: observations from electron microscope and electron-probe analysis.

Displacement or removal of mineral during the processing of calcified tissues for electron microscopy is a recognized phenomenon. An electron microscope analysis has been made of artefactual mineral loss during ultramicrotomy of osteogenic tissue. It is concluded from morphological investigation and the use of electron diffraction that this loss of crystalline mineral during sectioning can considerably change the morphology of calcified tissues and may lead to inaccurate interpretation of cell and matrix morphology. Electron probe X-ray microanalysis has been used to demonstrate in a semi-quantitative manner, the artefactual loss of calcium and phosphorus. Problems of specimen preparation for such analytical work are discussed.

Animals↗
PubMed1989

Separation of bone matrix proteins by calcium-induced precipitation.

It was found that significant precipitation occurred immediately after calcium, at a concentration as low as 2 mM, was added to a desalted solution of EDTA extract of adult bovine femur. The maximal yield of the precipitates was observed at a calcium concentration of 30 mM. These precipitates were dissolved in 0.5 M EDTA, desalted, and characterized by Sepharose CL-6B gel filtration chromatography and high performance gel-exclusion chromatography. Results revealed that the precipitates were enriched in a 40 K protein and a higher molecular weight fraction as compared with the original extract of bone proteins. The 40 K fraction was isolated and identified as osteonectin, as judged from amino acid analysis, electrophoresis, and immunodetection. The supernatant after calcium-induced precipitation predominantly contained osteocalcin and a 50 K protein that was tentatively identified as alpha 2HS protein. Osteonectin was purified from the calcium-induced precipitates from the EDTA extract of bovine bone. By calcium titration using fluorescence spectrometry, the isolated osteonectin showed high affinity to calcium ions with an apparent dissociation constant (K0.5) of 8 x 10(-7) M. Thus, the use of calcium to separate bone proteins, especially osteonectin, was proved to be a useful technique. In addition, calcium-induced precipitation of osteonectin suggested a possible in vivo mechanism via which osteonectin might interact with calcium ions and participate in the initial immobilization of calcium to induce the nucleation of calcification in bone tissue.

Animals↗
PubMed1995

Expression of bone matrix protein messenger ribonucleic acids in human breast cancers. Possible involvement of osteopontin in development of calcifying foci.

BACKGROUND: Development of calcifying foci is a fairly common finding in human breast cancers, and the deposition of calcium phosphate is observed in such foci. The calcium phosphate is a physiologic component of bones and teeth. Since the expression of messenger (m) RNAs of osteopontin (OPN), osteocalcin (OC), osteonectin (ON), and matrix gla protein (MGP) has been described in bones and teeth, we examined the mRNA expression of OPN, OC, ON, or MGP in the calcifying foci that were observed in human breast cancers. EXPERIMENTAL DESIGN: Cell types expressing mRNAs of OPN, ON or MGP were identified with combination of in situ hybridization and immunohistochemistry. RESULTS: The OPN mRNA-expressing cells clustered around the necrotic foci within cancer cell nests, and the examination with anti-OPN antibody revealed that OPN protein was localized in such necrotic foci where calcium phosphate deposited. The OPN mRNA-expressing cells were identified as macrophages by staining the adjacent section with the anti-CD68 PG-M1 monoclonal antibody which specifically recognizes macrophages. Neither ON mRNA-expressing cells nor MGP mRNA-expressing cells appeared to correlate with the deposition of calcium phosphate. CONCLUSIONS: The OPN protein produced by macrophages appeared to play a significant role for development of calcifying foci within necrotic area of breast cancers.

Antibodies, Monoclonal↗
PubMed1987

Demonstration that ethanol inhibits bone matrix synthesis and mineralization in the rat.

The effects of ethanol on bone and mineral metabolism were investigated in 3 groups of male rats. The first group received ethanol administered as 36% of caloric content in a liquid diet for 3 weeks. A second group of pair-fed animals was given the same liquid diet, except that sucrose was substituted isocalorically for ethanol. A third group of rats was fed standard laboratory chow. The ethanol-treated rats gained significantly less weight than laboratory chow-fed controls but gained the same weight as the pair-fed animals. Ethanol-treated rats had a modest but significant decrease in mean serum calcium compared to pair-fed controls (10.3 +/- 0.1 vs. 10.6 +/- 0.1 mg/dl, p less than .001). Mean serum phosphate, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D and immunoreactive parathyroid hormone were the same in the 3 groups. The ethanol-treated animals showed significant decreases in mean tibial length (1.88 +/- 0.01 vs. 1.98 +/- 0.02 cm, p less than .01), mean endosteal bone formation rate (0.0006 +/- 0.0001 vs. 0.0026 +/- 0.0003 mm3/day, p less than .001) and mean periosteal bone formation rate (0.022 +/- 0.001 vs. 0.026 +/- 0.001 mm3/day, p less than .01) compared to the pair-fed controls. The ethanol-treated rats demonstrated significant decreases in mean periosteal mineralization rate (7.5 +/- 0.3 vs. 10.3 +/- 0.6 micron/day, p less than .01) and mean periosteal apposition rate (8.5 +/- 0.5 vs. 11.0 +/- 0.8 micron/day, p less than .05) and a significant increase in mean periosteal osteoid thickness (15.5 +/- 1.4 vs. 10.4 +/- 0.8 micron, p less than .01) compared to pair-fed controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

The effect of long-term ovarian hormone deficiency on transforming growth factor-beta and bone matrix protein mRNA expression in rat femora.

Estrogen deficiency results in increased bone turnover and osteopenia. Decreased transforming growth factor beta (TGF-beta) has been implicated as having a role in ovariectomy (OVX)-induced bone loss; however the decrease in TGF-beta mRNA may simply be due to the reduction in cancellous bone volume that occurs following OVX. This investigation characterized the effect of long-term OVX (11.5 months) on mRNA levels for TGF-beta, osteocalcin (OC), and type I collagen (TYPE I) and expressed these data relative to the amount of cancellous bone surface. Additionally, the short-term effect of estrogen administration on TGF-beta, OC, and TYPE I mRNA was evaluated. OVX resulted in a 56% loss of bone surface. At the tissue level, TGF-beta was reduced, OC was increased, and TYPE I was unchanged. Expressed relative to bone surface, TGF-beta was unchanged and OC and TYPE I were significantly elevated. Four hours after estrogen administration, TGF-beta mRNA was unchanged compared to vehicle-treated controls. The data suggest that bone turnover is elevated after long-term OVX, but do not suggest a direct role of TGF-beta in OVX-induced bone loss.

Aging↗
PubMed1999

Expression of bone matrix proteins in urolithiasis model rats.

Urinary calcium stones are a pathological substance, and they show similarities to physiological mineralization and other pathological mineralizations. The expression of messenger (m) RNAs of osteopontin (OPN), matrix Gla protein (MGP), osteonectin (ON) and osteocalcin (OC) in bones and teeth has been described. We previously identified OPN as an important stone matrix protein. In addition, the spontaneous calcification of arteries and cartilage in mice lacking MGP was recently reported, a finding which indicates that MGP has a function as an inhibitor of mineralization. Here, we examined the mRNA expressions of OPN, MGP, ON, and OC in the kidneys of stone-forming model rats administered an oxalate precursor, ethylene glycol (EG) for up to 28 days. The Northern blotting showed that the mRNA expressions of OPN and MGP were markedly increased with the administration of EG, but their expression patterns differed. The OPN mRNA expression reached the maximal level at day 7 after the initiation of the EG treatment and showed no significant difference after 14 and 28 days, whereas the MGP mRNA expression rose gradually to day 28. The in situ hybridization demonstrated that the cell type expressing OPN mRNA was different from that expressing MGP. We suggest that OPN acts on calcification and MGP acts on suppression.

Animals↗
PubMed1993

Molecular interface characterization in human bone matrix. I. Biochemical and IR spectroscopic studies.

The aim of this work is the characterization of interfaces in calcified tissues. In order to separate the non-collagenous bone proteins, according to their interaction with collagen or hydroxyapatite crystals, 10 sequential bone demineralizations using EDTA alone were carried out, followed by four sequential extractions using both EDTA and GuHCl. The extracts were characterized by SDS-PAGE, IR spectrum analysis, and kinetics of demineralization and proteins released. A great proportion of non-collagenous proteins are bound to the collagen matrix, many of which have a high affinity to it. This work demonstrates that collagen is not directly linked to the mineralized phase.

Adult↗
PubMed2005

PGE2 induces the gene expression of bone matrix metalloproteinase-1 in mouse osteoblasts by cAMP-PKA signaling pathway.

Prostaglandin E2 (PGE2), an abundant eicosanoid in bone, has been implicated in a number of pathological states associated with bone loss, and is also known to stimulate matrix metalloproteinase (MMP)-1 synthesis and secretion in rat and human osteoblast cells, although the nature of the intracellular reaction remains unclear. Although MMP-1 plays a critical role in bone-remodeling, it would be of interest to examine whether PGE2 regulates MMP-1 expression by mouse osteoblasts or not. Here we demonstrate that PGE2 is a potent inducer of MMP-1 production in fetal osteoblasts and show that PGE2 stimulates the activity of the MMP-1 promoter in osteoblasts, suggesting that PGE2 controls MMP-1 gene expression at least at the transcriptional level. PGE2 induced MMP-1 messenger RNA (mRNA) expression in the cells within 4 h, and this expression was maintained for 36 h. The increase in MMP-1 production with 0.1-2.0 microM PGE2 was dose-dependent. We also found that PGE2 (1.5 microM) up-regulated MMP-1 protein levels in cultured mouse osteoblasts, as evidenced by ELISA. To examine whether PGE2 mediated response and signal pathway are involved in the intracellular action, the PGE2-mediated expression of the MMP-1 gene was investigated in mouse osteoblast cells. A Northern blot analysis showed that PGE2 and PGE1 were potent stimulators of MMP-1 transcription, and the presence of thromboxane B2 had no effect. The increase in MMP-1 transcript after PGE2 treatment was observed at 4h, reaching a maximum at 6h, and persisted for 24h. This response was dose-dependent. Cycloheximide, an inhibitor of protein synthesis, completely blocked this effect by PGE2, indicating that the expression of other genes is also required. The second messenger analog, 8-bromo-cAMP, mimicked the effects of PGE2 by stimulating a dose-dependent increase in MMP-1 mRNA levels, with a maximal effect that was quantitatively similar to that observed with PGE2. Thus, the present results strongly suggest that the PGE2 stimulation of MMP-1 synthesis is due to the activation of MMP-1 gene transcription and a subsequent marked increase in MMP-1 transcription. This effect is dependent on de novo protein synthesis and is mimicked by protein kinase A activation. The findings suggest that PGE2 is involved in the cAMP-PKA signaling pathway in regulating MMP-1 gene expression in osteoblasts.

Animals↗