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PubMed1997

How do plasma membranes reach the circulation?

Diagnostic enzymology measures the serum or plasma levels of enzymes that were originally located within the cell, or were attached to its plasma membrane with their active sites exposed to the external milieu. The process by which they are released varies under different physiological and pathological conditions. In this way, shedding of hepatocyte plasma membranes is thought to be responsible for the release of liver plasma membrane fragments (LiPMF) into the circulation in metastatic, infiltrative and cholestatic liver diseases. Several membrane-bound enzymes, such as gamma-glutamyltransferase (gamma-GT), alkaline phosphatase (ALP), leucine aminopeptidase (LAP) and 5'-nucleotidase (5'-Nu) are expressed at the surface of the shedded LiPMF. These enzymes are attached to the cell membrane by means of hydrophobic interactions between the anchoring domain of the enzyme and lipid components of the cell membrane, e.g. through a specific glycan phosphatidylinositol (GPI) anchor. There is a striking homology between these LiPMF and the membrane fragments shedded or actively formed by other cells, such as bone matrix vesicles-rich in bone ALP-, membrane fragments of the syncitiotrophoblast-rich in placental ALP-, and membrane fragments present in duodenal fluid-rich in intestinal ALP. With the exception of LiPMF, membrane-bound (Mem-) forms of ALP are only very exceptionally found in human serum. Normally, the soluble (Sol-ALP) dimeric fractions of the enzyme predominate in serum, but liver, bone, placental and intestinal ALP can also be present as GPI-anchor bearing (Anch-) hydrophobic isoforms. Models for the release in the circulation of Mem-, Anch- and Sol-liver and intestinal ALP, involving both plasma membrane-associated GPI-phospholipase-D (GPI-PLD) and liver bile salts are proposed.

5'-Nucleotidase↗

PubMed2002

TGF-beta1 secretion of ROS-17/2.8 cultures on NiTi implant material.

The biocompatibility of an orthopedic implant depends on the effect of the implant on bone-forming cells, osteoblasts. Changes in osteoblastic proliferation, maturation and differentiation are important events in ossification that enable monitoring the effect of the implant. Transforming growth factor-beta (TGF-beta) is known to suppress osteoblast proliferation and, on the other hand, to induce the maturation and differentiation of osteoblasts. Moreover, osteoblasts produce TGF-beta, which is embedded in the bone matrix and activated by bone-resorbing osteoclasts. TGF-beta inhibits osteoclastic activity. Here, we show for the first time the effect of nickel titanium shape memory metal (NiTi) on osteoblastic cytokine expression. In this study, we measured the levels of TGF-beta with enzyme-linked immunosorbent assay (ELISA) from a ROS-17/2.8 osteosarcoma cell line cultured on different metal alloy discs. ELISA results were proportioned to total DNA content of the samples. We compared NiTi, to stainless steel (Stst), pure titanium (Ti) and pure nickel (Ni). The TGF-beta1/DNA value in the NiTi group (0.0007 +/- 0.0003) was comparable with those seen in the Stst (0.0008 +/- 0.0001) and Ti (0.0007 +/- 0.0001) groups. The concentration in the Ni group was lower (0.0006 +/- 0.0003), though not statistically significantly so. In addition, the effect of surface roughness on TGF-beta1 production was studied. We compared three different grades of roughness in three differently hot-rolled alloys: NiTi. hot-rolled at 950 degrees C. Ti alloy hot-rolled at 850 degrees C (TiI) and the same Ti alloy hot-rolled at 1,050 degrees C (TiII). We found that increasing roughness of the NiTi surface increased the TGF-beta1 concentration. On the other hand, all roughness groups of TiII showed low levels of TGF-beta1. while a rough TiI surface induced similar TGF-beta1, expression as rough NiTi. Further, these same measurements made with interleukine 6 (IL-6) were found to be under the detection limit in these cultures. We conclude that a rough NiTi surface promotes TGF-beta1 expression in ROS-17/2.8 cells.

Animals↗

PubMed1999

The role of prostaglandins and nitric oxide in the response of bone to mechanical forces.

We have developed an experimental model whereby bone is exposed to a brief episode of mechanical stimulation, which is followed by bone formation. The earliest response is in osteocytes, which express c-fos and insulin-like growth factor (IGF-1) within 30-60min. Thirty-six to 72h after loading bone matrix gene expression occurs on bone surfaces. The osteogenic response can be suppressed by a single dose of nitric oxide synthase (NOS) or prostaglandin (PG) synthase inhibitors, if these are administered just before mechanical stimulation: similar doses after stimulation have no effect. There is a later phase of indomethacin-sensitivity associated with COX-2 expression in bone at 6h. Thus, mechanically induced osteogenesis involves early expression of c-fos and IGF-1 by osteocytes, which are believed to be the strain-sensitive cells in bone. Both NOS and PG synthase, either in parallel or in sequence, are crucial to the initial transduction of the mechanical stimulus into an osteogenic response.

Animals↗

PubMed2003

Three-dimensional trabecular alignment model.

Trabecular alignment theory has been used to quantify Wolff's Law of bone remodeling. A three-dimensional finite element scheme was developed to analyze the bone remodeling phenomenon. The mathematical model proposed by Mullender et al. and later modified by Smith et al. was adopted to simulate the surface-based trabecular resorption and formation processes. Enhancements incorporated into the previous model include: mapping into three-dimensions, controlling the remodeling signal's passage through marrow, controlling the finite distance the signal may pass through the bone matrix, and including non-bone material in the finite element model. After the model is explained and thoroughly studied, three-dimensional implant surface geometries are simulated.

Adaptation, Physiological↗

PubMed2006

Chemotactic migration of human mesenchymal stem cells and MC3T3-E1 osteoblast-like cells induced by COS-7 cell line expressing rhBMP-7.

During bone development, remodeling, and repair, bone morphogenetic proteins (BMPs) induce the differentiation of mesenchymal progenitor cells (MPCs) that enter into the osteoblastic lineage, and enhance the recruitment of MPCs and osteogenic cells. The process of migration is believed to be regulated, in part, by growth factors stored within the bone matrix, which are released by bone resorption. In this study, primary human mesenchymal stem cells (hMSCs) and MC3T3-E1 osteoblasts were examined for chemotaxis in response to recombinant human BMP-7 (rhBMP-7) produced in COS-7 cells (co-culture system). In order to produce BMP-7 transfected cells (BTCs), which serve as suppliers of rhBMP-7 under in vitro culture conditions, the encoding DNA was transferred into the pTARGET expression vector and introduced into COS-7 cells by conventional genetic engineering techniques. In cell culture studies, the rhBMP-7 produced in BTCs stimulated the specific activity of ALP, the production of cAMP in response to PTH, and the synthesis of osteocalcin. Migration assays were conducted with a computer-aided time-lapse video-microscopy system, to allow the rapid and precise analysis of cell migration and for the dynamic measurement of cell position and morphology. The migration distance and speed of the MC3T3-E1 cells, or hMSCs, co-cultured with BTCs, using a band-type seeding method, were significantly increased (p < 0.001), compared to those of the MC3T3-E1 cells (or hMSCs) only. In conclusion, these studies revealed that rhBMP-7 plays a role in the migration of bone-forming cells, and that the co-culture model (co-culture of bone-forming cells with BMP-7-producing cells) using a computer-aided, time-lapse video-microscopy system, is useful for the chemotactic migration assay of other chemotactic growth factors.

3T3 Cells↗

PubMed2003

Distribution of tenascin-c and -X in rat TMJ development.

In the neonatal and postnatal development of rat TMJ, tenascin-C and -X were detected in the muscle, bone matrix, connective tissue around the bone, and blood vessel of rats at E18 (18-days old embryo), 0-, and 5-days postnatal. The reaction of tenascin-X was also found in the connective tissue around the mandibular condyle. The mRNA of tenascin-C (600 bp) and -X (588 bp) was also detected in the developmental muscle with the level of tenascin-C mRNA moderately decreased during development. Therefore, tenascin-C and -X may have different effects on the connective tissue during development of TMJ.

Animals↗

PubMed1996

BMP-2 for intramuscular bone induction: effect in squirrel monkeys is dependent on implantation site.

Demineralized bone matrix (DBM) reproducibly induces extraskeletal bone formation in rodents, but its effects in dogs and primates are negative or uncertain. In previous studies on the squirrel monkey, DBM did not induce bone, although the same implants were effective in rats. DBM implants augmented with recombinant human bone morphogenetic protein-2 (rhBMP-2) induced intramuscular bone formation in squirrel monkeys. However, the amount of induced bone was often minimal and sometimes absent. One explanation of this weak and unpredictable effect could be reactions to cellular components of the allogeneic DBM that was used as carrier. Therefore, we now repeated the experiment, using bovine type 1 collagen as carrier. 48 collagen discs (10 mm diameter), containing 0, 10, 40 or 200 microgram rhBMP-2, were implanted in 6 monkeys and 6 rats. The BMP-2 implants induced dose-dependent amounts of intramuscular bone in rats whereas, in squirrel monkeys, macroscopic bone induction occurred in less than half of the BMP-2 implants. There was no dose-dependency. Whether bone was formed or not was significantly influenced by individual variation among the monkeys, and by implant location within the muscle. Implants close to the muscle aponeurosis more often induced bone than did purely intramuscular ones. In this small series, we could not demonstrate a significant effect of BMP-2, as compared to control implants. Presumably there were too few cells expressing BMP-2 receptors in the only minimally traumatized muscle of these monkeys.

Animals↗

PubMed2000

Orthodontically stressed periodontium of transgenic mouse as a model for studying mechanical response in bone: The effect on the number of osteoblasts.

A better understanding of cellular and molecular mechanisms involved in response to mechanical stress is a prerequisite for future improvements in orthodontic treatment. To expand the application of molecular biology techniques in this area of research, we developed and characterized a mouse tooth movement model. The aim of this study was to biomechanically characterize this model and to evaluate the effect of orthodontic stress on the proliferation of periodontal osteoblasts. We used an orthodontic coil spring appliance with a low force/deflection rate, which produced an average force of 10-12 g. This design provided a predictable tipping movement of the molar with the center of rotation at the level of root apices. Histological observations of paradental tissues revealed a response favoring a fast onset of tooth movement and deposition of new osteoid starting after 3 days of treatment. The effect of treatment on the histomorpometric parameter of the number of osteoclasts per unit bone perimeter was determined after 1, 2, 3, 4, 6, and 12 days of treatment. Starting with day 2, the osteoblast number showed a modest but consistent increase in treated periodontal sites at all time-points, ranging from 14 to 39% and becoming significant only at day 6. Only a moderate increase in the number of osteoblasts in the areas of otherwise intense bone matrix synthesis suggests that, during bone formation, proliferation of cells has a smaller role compared to a marked increase in differentiation of individual cells. The mouse model, which allows for a controlled, reproducible, orthodontic mechanical loading, can be applied to both wild-type and transgenic animals and should enhance the research of the transduction of mechanical orthodontic signal into a biological response.

Journal Article↗

PubMed2000

Orthodontically stressed periodontium of transgenic mouse as a model for studying mechanical response in bone: The effect on the number of osteoblasts.

Journal Article↗

PubMed2005

Bone graft alternatives in the treatment of benign bone tumors.

Most bone grafting procedures are done during spinal fusion and to treat patients with skeletal trauma. Very few studies have addressed the bone grafting of skeletal defects after benign bone tumor excision. Contained defects have been treated with autogenous bone grafts, fresh-frozen allografts, freeze-dried allografts, demineralized bone matrix, and ceramic materials. Additionally, bone morphogenetic proteins may provide a future treatment option for bone tumor reconstruction.

Bone Neoplasms↗

PubMed1994

Dephosphorylation of osteopontin and bone sialoprotein by osteoclastic tartrate-resistant acid phosphatase. Modulation of osteoclast adhesion in vitro.

The tartrate-resistant acid phosphatase (TRAP) of skeletal osteoclasts was found to partially dephosphorylate the bone matrix phosphoproteins osteopontin (OPN) and bone sialoprotein (BSP). TRAP also partially dephosphorylated metabolically [32P]PO4-labeled OPN as well as BSP, whereas comparable amounts of either alkaline phosphatase or prostatic acid phosphatase, at their respective pH optima, were ineffective, indicating a certain preference of TRAP for these phosphoprotein substrates. It has previously (Flores, M., Norgärd, M., Heinegård, D., Reinholt, F. P., and Andersson, G. (1992) Exp. Cell Res. 201, 526-530) been shown that osteoclasts bind to OPN as well as to BSP coated onto glass. We can now show that the partially dephosphorylated proteins no longer support osteoclast binding. These results indicate that the secretion of TRAP from osteoclasts into the resorption area could exert a regulatory influence on the attachment of the cells to the bone surface. This could imply roles in the development of ruffled borders and/or in the regulation of osteoclast motility on the bone surface.

Acid Phosphatase↗

PubMed1998

Gingival crevicular fluid from patients with periodontitis contains bone resorbing activity.

Inflammatory processes occurring in the vicinity of bone tissue often result in stimulation of osteoclast activity and loss of skeletal mass. The aim of the current study was to determine if inflammatory exudates collected from gingival pockets in patients with periodontitis contain factors capable of stimulating resorptive activity. The degree of bone mineral mobilization and bone matrix degradation was assessed by analysis of the release of 45Ca and 3H from bones prelabelled with 45CaCl2 and [3H]proline, respectively. Gingival crevicular washings from six patients with signs of periodontitis stimulated 45Ca or 3H release from the calvarial bones. The stimulatory effect of the gingival crevicular washings on 45Ca release was concentration- and time-dependent, and reduced by calcitonin, a specific osteoclast inhibitor. These data demonstrate that crevicular fluid contains factor(s) which can stimulate osteoclastic degradation of bone in vitro. The bone resorbing activity was partially retained after extensive dialysis. Analysis of the concentrations of prostaglandin E2, interleukin-1alpha and interleukin-1beta in the crevicular fluids, and comparisons of these agents as stimulators of 45Ca release in the mouse calvarial assay, suggest that prostaglandin E2 is not the sole factor responsible for the bone resorbing activity of the exudates. The data indicate that other factors, such as IL-1, may play key roles in the stimulation of osteoclastic activity by gingival crevicular washings.

Adolescent↗

PubMed2003

[Clinical application of tissue engineered bone repair of human craniomaxillofacial bone defects].

OBJECTIVE: To explore the feasibility of tissue engineered bone formation in human being using human bone marrow stromal cells (hBMSCs) and the possibility of clinical repair of craniomaxillofacial bone defects with tissue engineered bone. METHODS: Total 11 patients of cranial defects and aperture piriformis bone depression were included in this study. The hBMSCs were isolated by Percoll gradient centrifugation from patient's bone marrow aspirated from iliac crest. The hBMSCs were cultured in vitro and induced to become osteogenic cells in the DMEM medium containing 10% self-serum, beta-glycerophosphate (10 nmol/L) dexamethasone (10(-8) mol/L), L-2-ascorbic acid (50 micro mol/L), and 1, 25 (OH)(2)VD(3)(10 nmol/L). Induced hBMSCs of passage 3 were harvested and seeded onto partly demineralized allogenic bone matrix (pDBM) to form a cell-scaffold construct and in vitro co-culture for 1 week. The defects were repaired with the cell-scaffold construct. In 3 cases of aperture piriformis bone depression, one side was repaired with hBMSC/pDBM, while the other side was repaired by pDBM alone. All cases were followed up for 1, 3, 6 months post-operation as short-term evaluation and 1 to 2.5 years post-operation as long-term evaluation by three-dimensional computerized tomography (3D-CT) and clinical examination. In 2 cases who received secondary surgery, extra engineered bone tissue and control pDBM were harvested at the implantation sites for histological examination and immunohistochemistry. RESULTS: 3D-CT demonstrated that engineered bone was formed in 3 to 6 months post-operation. Additionally, formed bone maintained stable up to 1 - 2 years without absorption. Histologically, engineered bones revealed their structures similar to that of normal bone in HE staining. Interestingly, endochondral ossification was also observed in engineered bone. Immunohistochemistry shows positive staining of osteonectin and osteocalcin in engineered and normal bones. In contrast, implanted pDBM was completely degraded in 3 - 6 months as revealed by 3D-CT. Histologically, degraded pDBM and fibrous tissue were observed in the sites where pDBM alone was implanted. CONCLUSIONS: Tissue engineered bone can be formed in human being. Engineered bone can be used to repair clinical bone defect with satisfactory result. Furthermore, the result of this study proves that tissue engineered bone is possible for clinical application.

Adolescent↗

PubMed1988

Effect of phosphorus supplementation on bone formation induced by osteosarcoma-derived bone-inducing substance in X-linked hypophosphatemic mice.

In our previous report, we demonstrated normal cartilage and bone matrix formation and a defect of bone mineralization in hypophosphatemic (Hyp) mice using an ectopic bone formation system. That system consisted of an osteogenic sarcoma-derived bone-inducing substance. In this report, we describe the effect of phosphorus supplementation on abnormal bone mineralization. The osteogenic sarcoma-derived bone-inducing substance was implanted in Hyp mice or control mice. The Hyp mice were divided into two groups after implantation. One group was fed a normal laboratory chow, while the other was fed a high-phosphorus diet for 4 weeks of the experimental period. Normal control mice were fed the normal laboratory chow. The mean serum phosphorus level in the high-phosphorus diet group was normal at 2, 3 and 4 weeks after implantation. Using the method of 85Sr incorporation, the high-phosphorus diet group showed marked improvement in bone mineralization at 2 and 4 weeks after implantation, but incomplete improvement at 3 weeks. On the other hand, histological study of the high-phosphorus diet group at 4 weeks after implantation still showed a meaningful amount of the osteoid matrix formation compared to the control. These findings suggest that the abnormal bone mineralization in Hyp mice was mainly due to their abnormally low serum phosphorus level. However, still other abnormalities might exist and these might be responsible for the incomplete improvement in bone mineralization.

Animals↗

PubMed1987

Tenascin is associated with chondrogenic and osteogenic differentiation in vivo and promotes chondrogenesis in vitro.

The tissue distribution of the extracellular matrix glycoprotein, tenascin, during cartilage and bone development in rodents has been investigated by immunohistochemistry. Tenascin was present in condensing mesenchyme of cartilage anlagen, but not in the surrounding mesenchyme. In fully differentiated cartilages, tenascin was only present in the perichondrium. In bones that form by endochondral ossification, tenascin reappeared around the osteogenic cells invading the cartilage model. Tenascin was also present in the condensing mesenchyme of developing bones that form by intramembranous ossification and later was present around the spicules of forming bone. Tenascin was absent from mature bone matrix but persisted on periosteal and endosteal surfaces. Immunofluorescent staining of wing bud cultures from chick embryos showed large amounts of tenascin in the forming cartilage nodules. Cultures grown on a substrate of tenascin produced more cartilage nodules than cultures grown on tissue culture plastic. Tenascin in the culture medium inhibited the attachment of wing bud cells to fibronectin-coated substrates. We propose that tenascin plays an important role in chondrogenesis by modulating fibronectin-cell interactions and causing cell rounding and condensation.

Animals↗

PubMed1994

Localization of follistatin, an activin-binding protein, in bone tissues.

We have previously reported that activin-A has a mitogenic effect on osteoblast-like MC3T3-E1 cells and that these cells produce an activin-binding protein, follistatin (Hashimoto, M., Shoda, A., Inoue, S., Yamada, R., Kondo, T., Sakurai, T., Ueno. N., and Muramatsu, M. (1992) J. Biol. Chem. 267, 4999-5004). Activin-A was also detected abundantly in bone matrix tissues and was found to act as an osteoclast differentiation factor. Here, we studied the expression of follistatin in bone tissues by in situ hybridization with a follistatin cRNA probe. Follistatin transcript was detected in the osteoblasts and a fraction of osteocyte population in the developing mouse mandible. Immunohistochemistry using anti-follistatin antibody supported this observation at the protein level. Follistatin mRNA was also detected in the callus of repairing bone after fracture. These findings suggest that activin and follistatin may play significant roles in the bone system in vivo.

Animals↗

PubMedDate not supplied

[Mineral phase and protein matrix status of rat bony tissue after a flight on the Kosmos-1129 biosatellite].

The major parameters of the mineral component and protein matrix of bones were investigated in 30 rats flown onboard Cosmos-1129. Postflight, the content of calcium decreased by 7.8%, that of phosphorus diminished by 11.8%, the Ca/P ratio increased by 5.9%, the content of collagen diminished by 14.7% and that of non-collagenous proteins by 45.7% and the content of sialic and hexuronic acids increased by 36.2% and 14.6%, respectively, as compared to the vivarium controls. The paper discusses the role of EDTA-and HCl-protein extracts, soluble and poorly soluble calcium fractions, protein-Ca-phosphate complex, sialic and hexuronic acids in the mechanism of calcium binding by the bone organic matrix.

Animals↗

PubMed2001

Macrophage migration inhibitory factor up-regulates matrix metalloproteinase-9 and -13 in rat osteoblasts. Relevance to intracellular signaling pathways.

Neutral matrix metalloproteinases (MMPs) play an important role in bone matrix degradation accompanied by bone remodeling. We herein show for the first time that macrophage migration inhibitory factor (MIF) up-regulates MMP-13 (collagenase-3) mRNA of rat calvaria-derived osteoblasts. The mRNA up-regulation was seen at 3 h in response to MIF (10 microg/ml), reached the maximum level at 6-12 h, and returned to the basal level at 36 h. MMP-13 mRNA up-regulation was preceded by up-regulation of c-jun and c-fos mRNA. Tissue inhibitor of metalloproteinase (TIMP)-1 and MMP-9 (92-kDa type IV collagenase) were also up-regulated, but to a lesser extent. The MMP-13 mRNA up-regulation was significantly suppressed by genistein, herbimycin A and 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine. Similarly, a selective mitogen-activated protein kinase (MAPK) kinase (MEK)1/2 inhibitor (PD98059) and c-jun/activator protein (AP)-1 inhibitor (curcumin) suppressed MMP-13 mRNA up-regulation induced by MIF. The mRNA levels of c-jun and c-fos in response to MIF were also inhibited by PD98059. Consistent with these results, MIF stimulated phosphorylation of tyrosine, autophosphorylation of Src, activation of Ras, activation of extracellular signal-regulated kinases (ERK) 1/2, a MAPK, but not c-Jun N-terminal kinase or p38, and phosphorylation of c-Jun. Osteoblasts obtained from calvariae of newborn JunAA mice, defective in phosphorylation of c-Jun, or newborn c-Fos knockout (Fos -/- ) mice, showed much less induction of MMP-13 with the addition of MIF than osteoblasts obtained from wild-type or littermate control mice. Taken together, these results suggest that MIF increases the MMP-13 mRNA level of rat osteoblasts via the Src-related tyrosine kinase-, Ras-, ERK1/2-, and AP-1-dependent pathway.

Animals↗