Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Titanium (Ti) surfaces with rough microtopographies enhance osteogenic differentiation, local factor production, and response to osteogenic agents in vitro and increase pullout strength of dental implants in vivo. Estrogens regulate bone formation, resorption, and remodeling in females and may be important in implant success. Here, we tested the hypothesis that estrogen modulates osteoblast response to implant surface morphology. Primary female human osteoblasts were cultured to confluence on three Ti surfaces (pretreatment, PT - R(a) 0.60 microm; sandblasted and acid-etched, SLA - R(a) 3.97 microm; and Ti plasma-sprayed, TPS - R(a) 5.21 microm) and treated for 24 h with 10(-7) or 10(-8) M 17beta-estradiol (E(2)). Cell number decreased with increasing surface roughness, but was not sensitive to E(2). Alkaline phosphatase specific activity of isolated cells and cell layer lysates was lower on rough surfaces. E(2) increased both parameters on smooth surfaces, whereas on rough surfaces, the stimulatory effect of E(2) on alkaline phosphatase was evident only when measuring cell layer lysates. Osteocalcin levels were higher in the conditioned media of cells grown on rough surfaces; E(2) had no effect in cultures on the plastic surfaces, but increased osteocalcin production on all Ti surfaces. TGF-beta1 and PGE(2) production was increased on rough surfaces, and E(2) augmented this effect in a synergistic manner; on smooth surfaces, there was no change in production with E(2). The response of osteoblasts to surface topography was modulated by E(2). On smooth surfaces, E(2) affected only alkaline phosphatase, but on rough surfaces, E(2) increased levels of osteocalcin, TGF-beta1, and PGE(2). These results show that normal adult human female osteoblasts are sensitive to surface microtopography and that E(2) can alter this response.
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PMID:Response of normal female human osteoblasts (NHOst) to 17beta-estradiol is modulated by implant surface morphology. 1220 40

In our previous study, we have validated the efficacy and the safety of Gu-Sui-Bu [Drynaria fortunei (Kunze) J. Sm.] by the bone cells culture. However, a satisfactory delivery system for Gu-Sui-Bu must be developed before it can be used in clinical medicine. In this study, we try to use modified calcium hydrogenphosphate (MCHP) bioceramic as a carrier to transport Gu-Sui-Bu into the bone cell culture system. Toward this goal, we evaluated the effect of a Gu-Sui-Bu-immobilized modified calcium hydrogenphosphate (GI-MCHP) on the bone cells activities. THE CHINESE MEDICINE: Gu-Sui-Bu [Drynaria fortunei (kunze) J. Sm] was extracted and then immobilized on the surface of MCHP. The rat osteoblasts-osteoclasts co-culture system was used as the experimental model. After the cells grew to 80% confluence, different sizes of GI-MCHP particles were tested. The mitochondria activity of the bone cells after exposure was determined by colorimetric assay. Biochemical markers such as lactate dehydrogenase (LDH), alkaline phosphatase (ALP), acid phosphatase (ACP) and prostaglandin E(2) titer were analyzed to evaluate the bone cells activities. Histomorphometric study of osteoclasts activities and the phenotype expression of osteoblasts were also evaluated. There is no detectable titer of LDH secretion into the medium and no significant change in the intracellular ALP content. The ALP titer in the culture medium did increase significantly at 3 days' culture, while there is a significant decrease in the intracellular ACP content and significant increase in the ACP titer in the medium. The concentrations of PGE(2) in tested medium are always significantly higher than that of control medium during the 7 days' culture. At the end of 7 days' culture, the PGE(2) concentrations in the tested medium were still 4.74 times that of the control medium. After GI-MCHP treatment on bone cells, the size of the osteoclasts seems decreased and their cell integrity seems lost, while the osteoblasts phenotype expression was relatively preserved. From this study, we demonstrated that Gu-Sui-Bu [Drynaria fortunei (Kunze) J. Sm.] immobilized MCHP has well preserved the potential beneficial effects of Gu-Sui-Bu on the bone cells culture.
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PMID:The effect of Gu-Sui-Bu (Drynaria fortunei J. Sm) immobilized modified calcium hydrogenphosphate on bone cell activities. 1248 5

Implant surface morphology regulates osteoblast phenotypic expression. Osteoblast sensitivity to non-biologic surfaces suggests that native bone surface features may also affect osteoblast response. To test this, MG63 osteoblast-like cells were grown for 7 days on bovine cortical bone wafers pretreated with rat bone marrow osteoclasts for 0, 10 or 20 days. Response to osteoclast-treated surfaces was compared to the response of MG63 cells to titanium surfaces with smooth and rough microtopographies. Cell number, differentiation (alkaline phosphatase activity and osteocalcin levels), and local factors (PGE(2) and TGF-beta1) were measured in confluent cultures. Compared to culture on plastic, cell number was reduced on all three types of bone wafers; this effect was dose-dependent with increasing resorption of the surface. Alkaline phosphatase specific activity was increased (P<or=0.05) on all three surfaces compared with plastic, but this increase was not dependent on resorption time, indicating this parameter was sensitive to the surface (bovine bone vs. plastic) but not to osteoclast-resorption. There was a direct correlation between the area of the bone surface resorbed and the amount of osteocalcin, TGF-beta1 and PGE(2) (R(2)=0.8025, 0.8689, 0.8896, respectively). With 20 days of osteoclast pretreatment, there was a 20-fold increase in osteocalcin over plastic and a 7-fold increase over cultures on untreated bone wafers. Similar increases were found for TGF-beta1 and PGE(2). Thus, surface changes resulting from osteoclast pretreatment have a strong effect on osteoblast phenotypic expression, and suggest that microtopography may play a role.
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PMID:Pretreatment of bone with osteoclasts affects phenotypic expression of osteoblast-like cells. 1279 63

The underlying mechanisms responsible for both cartilage loss and subchondral bone changes in osteoarthritis (OA) remain unknown. It is becoming recognized that the extracellular matrix influences the metabolism of cells both in vivo and in vitro and can modify their responses to external stimuli. Indeed, the glycosaminoglycan/proteoglycan matrix is of major importance for the proliferation and/or differentiation of a number of cells. Here, we determined the potential role of hyaluronic acid (HA) of increasing molecular weight (MW) to alter the expression of metabolic markers and cytokine production by human osteoarthritic (OA) subchondral osteoblasts (Ob). Both 1,25(OH)(2)D(3)-induced alkaline phosphatase activity (ALPase) and osteocalcin release were increased in OA Ob when compared to normal. HA reduced osteocalcin release in OA Ob at MW of 300 and above, whereas HA failed to significantly modify ALPase. Parathyroid hormone (PTH) stimulated cyclic AMP (cAMP) formation by OA Ob. HA had a biphasic effect on this PTH-dependent activity, totally inhibiting cAMP formation at MW of 300 and 800. HA of increasing MW progressively reduced the levels of Prostaglandin E(2) (PGE(2)) and interleukin-6 (IL-6) produced by OA Ob. Interestingly, urokinase plasminogen activator (uPA) and and PA inhibitor-1 (PAI-1) levels were not significantly affected by HA of increasing MW; however, the PAI-1 to uPA ratio showed a slight, yet nonsignificant increase. Surprisingly, uPA activity was increased in OA Ob under the same conditions. Last, HA had no effect on the production of insulin-like growth factor-1 by these cells. Our data suggest that high MW HA can modify cellular parameters in OA Ob that are increased when compared to normal. The effect of HA on inflammatory mediators, such as PGE(2) and IL-6, and on uPA activity is more striking at higher MW as well. Taken together, these results could suggest that HA of increasing MW has positive effects on OA Ob by modifying their biological synthetic capacities.
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PMID:Hyaluronic acid reverses the abnormal synthetic activity of human osteoarthritic subchondral bone osteoblasts. 1455 76

Osteoblasts exhibit a more differentiated morphology on surfaces with rough microtopographies. Surface effects are often mediated through integrins that bind the RGD motif in cell attachment proteins. Here, we tested the hypothesis that modulating access to RGD binding sites can modify the response of osteoblasts to surface microtopography. MG63 immature osteoblast-like cells were cultured on smooth (Ti sputter-coated Si wafers) and rough (grit blasted/acid etched) Ti surfaces that were modified with adsorbed monomolecular layers of a comb-like graft copolymer, poly-(L-lysine)-g-poly(ethylene glycol) (PLL-g-PEG), to limit nonspecific protein adsorption. PLL-g-PEG coatings were functionalized with varying amounts of an integrin-receptor-binding RGD peptide GCRGYGRGDSPG (PLL-g-PEG/PEG-RGD) or a nonbinding RDG control sequence GCRGYGRDGSPG (PLL-g-PEG/PEG-RDG). Response to PLL-g-PEG alone was compared with response to surfaces on which 2-18% of the polymer sidechains were functionalized with the RGD peptide or the RDG peptide. To examine RGD dose-response, peptide surface concentration was varied between 0 and 6.4 pmol/cm(2). In addition, cells were cultured on uncoated Ti or Ti coated with PLL-g-PEG or PLL-g-PEG/PEG-RGD at an RGD surface concentration of 0.7 pmol/cm(2), and free RGDS was added to the media to block integrin binding. Analyses were performed 24 h after cultures had achieved confluence on the tissue culture plastic surface. Cell number was reduced on smooth Ti compared to plastic or glass and further decreased on surfaces coated with PLL-g-PEG or PLL-g-PEG/PEG-RDG, but was restored to control levels when PLL-g-PEG/PEG-RGD was present. Alkaline phosphatase specific activity and osteocalcin levels were increased on PLL-g-PEG alone or PLL-g-PEG/PEG-RDG, but PLL-g-PEG/PEG-RGD reduced the parameters to control levels. On rough Ti surfaces, cell number was reduced to a greater extent than on smooth Ti. PLL-g-PEG coatings reduced alkaline phosphatase and increased osteocalcin in a manner that was synergistic with surface roughness. The RDG peptide did not alter the PLL-g-PEG effect but the RGD peptide restored these markers to their control levels. PLL-g-PEG coatings also increased TGF-beta1 and PGE(2) in conditioned media of cells cultured on smooth or rough Ti; there was a 20x increase on rough Ti coated with PLL-g-PEG. PLL-g-PEG effects were inhibited dose dependently by addition of the RGD peptide to the surface. Free RGDS did not decrease the effect elicited by PLL-g-PEG surfaces. These unexpected results suggest that PLL-g-PEG may have osteogenic properties, perhaps correlated with effects that alter cell attachment and spreading, and promote a more differentiated morphology.
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PMID:RGD-containing peptide GCRGYGRGDSPG reduces enhancement of osteoblast differentiation by poly(L-lysine)-graft-poly(ethylene glycol)-coated titanium surfaces. 1476 25

The effect of beta-cryptoxanthin, which is greatly present in fruits, has not been clarified so far on bone metabolism. The effect of beta-cryptoxanthin on bone formation and bone resorption was investigated in tissue culture in vitro. Rat femoral-diaphyseal (cortical bone) and -metaphyseal (trabecular bone) tissues were cultured for 48 h in Dulbecco's modified Eagle's medium (high glucose, 4.5%) supplemented with antibiotics and bovine serum albumin. The experimental cultures contained 10(-8)-10(-5) M beta-cryptoxanthin. The presence of beta-cryptoxanthin (10(-6) or 10(-5) M) caused a significant increase in calcium content, alkaline phosphatase activity and deoxyribonucleic acid (DNA) content in the diaphyseal and metaphyseal tissues. These increases were completely prevented in the presence of cycloheximide (10(-6) M), an inhibitor of protein synthesis. beta-Carotene (10(-6) or 10(-5) M) or xantine (10(-6) or 10(-5) M) had no effect on the diaphyseal and metaphyseal calcium contents. The bone-resorbing factors parathyroid hormone (1-34) (PTH; 10(-7) M) or prostaglandin E2 (PGE2; 10(-5) M) caused a significant decrease in calcium content in the diaphyseal and metaphyseal tissues. The decrease in bone calcium content induced by PTH or PGE2 was completely inhibited by beta-cryptoxanthin (10(-8)-10(-6) M). In addition, beta-cryptoxanthin (10(-8)-10(-6) M) completely inhibited the PTH (10(-7) M)- or PGE, (10(-5) M)-induced increase in medium glucose consumption and lactic acid production by diaphyseal and metaphyseal tissues. The inhibitory effect of beta-cryptoxanthin (10(-7) M) on PTH (10(-7) M)- or PGE2 (10(-5) M)-stimulated decrease in the diaphyseal calcium content was significantly prevented in the presence of 10(-3) M vanadate, an inhibitor of protein tyrosine phosphatase. Vanadate (10(-3) M) did not have a significant effect on calcium content and lactic acid production in control bone tissues. The present study demonstrates that beta-cryptoxanthin has a direct stimulatory effect on bone formation and an inhibitory effect on bone resorption in tissue culture in vitro.
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PMID:beta-Cryptoxanthin stimulates bone formation and inhibits bone resorption in tissue culture in vitro. 1503 Jan 78

Prostaglandins are now recognized to be important regulators for both bone formation and resorption. Among them, prostaglandin E(1) (PGE(1)) has been reported to stimulate cAMP accumulation and to induce alkaline phosphatase (ALP) activity, a marker of differentiation, in osteoblast-like cells. Recently, we have shown that p38 mitogen-activated protein (MAP) kinase pathway regulates ALP activity in response to activation of Gi protein-coupled receptors in mouse osteoblast-like MC3T3-E1 cells (Suzuki et al., Endocrinology 140 (1999) 3177). In the present study, we investigated whether p38 MAP kinase is involved in ALP activation by PGE(1) in MC3T3-E1 osteoblast-like cells. PGE(1) dose-dependently enhanced ALP activities in the concentration range between 1 nM and 1 microM in MC3T3-E1 cells. SB203580, a specific inhibitor of p38 MAP kinase, blocked the increase in ALP activity induced by PGE(1). Further analysis with western blotting suggested that PGE(1) induced an increase in tyrosine (Tyr) phosphorylation of p38 MAP kinase. Both Bt(2)cAMP, a permeable analogue of cAMP, and forskolin, which directly activates adenylate cyclase, also induced an increase in Tyr phosphorylation of p38 MAP kinase. H-89, a potent inhibitor of protein kinase A (PKA), significantly suppressed PGE(1)-induced Tyr phosphorylation of p38 MAP kinase. The results of this study suggest that PGE(1) stimulates p38 MAP kinase through the activation of PKA, resulting in the enhancement of ALP activity.
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PMID:Possible involvement of p38 MAP kinase in prostaglandin E1-induced ALP activity in osteoblast-like cells. 1506 50

Decidualisation of uterine stromal cells is a prerequisite for implantation of the embryo in mice. Here we have used an in vitro culture system in which stromal cells decidualise as indicated by a number of markers, including an increase in alkaline phosphatase (ALP) activity. The latter was used as a quantitative marker of decidualisation in the presence of low (2%) fetal calf serum. Prostaglandin E(2) (PGE(2)), which is known to induce decidualisation, increased ALP activity, and this effect was blocked in a dose-dependent manner by indomethacin. Leukemia inhibitory factor (LIF) was then examined, but it had no effect on PGE(2) secretion. However, LIF suppressed ALP activity in a dose-dependent manner in the presence of 2% serum, while an inhibitor of LIF that competes for binding to its receptor reversed the effect of LIF and increased ALP activity above the control level. In serum-free cultures, stromal cells differentiated rapidly, and no differences were observed between LIF-treated and untreated cultures. Stromal cells produce LIF during in vitro culture, and this peaked at 48 h. Freshly collected stromal cells from both day-2 and -4 pregnant mice expressed mRNA for the LIF receptor, and the transcript level was higher in cells isolated on day 4. However, no differences were observed in the relative levels of transcripts in cells from day 2 and day 4 after culture, nor were there differences between the LIF-treated cultures and controls. Therefore, in this study, we have shown that LIF suppresses decidualisation of murine uterine stromal cells in the presence of serum, this is not due to the regulation of PGE(2) secretion by stromal cells.
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PMID:Role of leukemia inhibitor factor (LIF) in decidualisation of murine uterine stromal cells in vitro. 1517 96

Deformation of the bone matrix by mechanical strain causes fluid shifts within the osteocytic canaliculi which affect osteocytic cell metabolism. We applied low fluid shear (1 - 63 micro Pa for 10 - 48 h) to human osteoblastic cells (HOB) in vitro to study its impact on cell proliferation and differentiated functions. Proteins involved in translating the physical force into a cellular response were characterised. Low fluid shear stress stimulated proliferation of HOB 1.2-fold when stress was applied intermittently for 24 h. Shear stress also increased differentiated cellular properties such as alkaline phosphatase (ALP) activity (121 % of control), fibronectin (FN) and fibronectin receptor (FNR) expression (290 % and 200 %, respectively). Prostaglandin E (2) (PGE (2)) and TGFbeta1 release into the medium were significantly stimulated when shear stress was applied for 6 - 12 h and 24 - 48 h, respectively. TGFbeta1 + 2 neutralising antibodies or the presence of indomethacine inhibited the mitogenic effect of fluid shear and reduced ALP activity to its control level. Furthermore, TGFbeta treatment induced a dose-dependent increase in FN and FNR expression. Therefore, fluid shear stress of low magnitude (a) suffices to affect HOB metabolism and (b) regulates anchorage of HOB via FN and FNR by stimulating osteoblastic PGE (2) and TGFbeta secretion.
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PMID:Fluid shear of low magnitude increases growth and expression of TGFbeta1 and adhesion molecules in human bone cells in vitro. 1523 20

Microtextured titanium implant surfaces enhance bone formation in vivo and osteoblast phenotypic expression in vitro, but the mechanisms are not understood. To determine the roles of specific microarchitectural features in modulating osteoblast behavior, we used Ti surfaces prepared by electrochemical micromachining as substrates for MG63 osteoblast-like cell culture. Cell response was compared to tissue culture plastic, a sand-blasted with large grit and acid-etched surface with defined mixed microtopography (SLA), polished Ti surfaces, and polished surfaces electrochemically machined through a photoresist pattern to produce cavities with 100, 30 and 10 microm diameters arranged so that the ratio of the microscopic-scale area of the cavities versus the microscopic-scale area of the flat region between the cavities was equal to 1 or 6. Microstructured disks were acid-etched, producing overall sub-micron-scale roughness (Ra=0.7 microm). Cell number, differentiation (alkaline phosphatase; osteocalcin) and local factor levels (TGF-beta1; PGE(2)) varied with microarchitecture. 100 microm cavities favored osteoblast attachment and growth, the sub-micron-scale etch enhanced differentiation and TGF-beta1 production, whereas PGE(2) depended on cavity dimensions but not the sub-micron-scale roughness.
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PMID:Differential regulation of osteoblasts by substrate microstructural features. 1557 58


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