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Osteoblast cells

Bone maintenance during adulthood is dependent on the equilibrium between bone formation by osteoblast cells and bone resorption by osteoclast cells. Bone loss with age is linked to increased osteoclast activity compared to... [Pg.97]

Osteoblasts Cells involved in bone formation during the remodeling... [Pg.1573]

Caryophyllidae are an interesting source of oligosaccharides and peptides with potential anti-inflammatory and/or immunomodulating effect. These polar compounds might for instance explain the fact that the fresh juice expressed from Aerva lanata (L.) Juss. (Amaranthaceae) inhibits carrageenan-induced edema in rodent. Note that the seeds of Gomphrena species inhibit the formation of IL-6 by osteoblastic cells (MC3T3-E10) without cytotoxicity in vitro. Such property could be useful for the treatment of chronic rheumatoid arthritis, infection, and cancer. In the Lauraceae, trans-cinnamal-dehyde from Cinnamomum cassia (Lauraceae, order Laurales) inhibits in vitro the... [Pg.62]

Tutak, W. et al. (2009) Toxicity induced enhanced extracellular matrix productionin osteoblastic cells cultured on single-walled carbon nanotube networks. Nanotechnology, 20 (25). 255101. [Pg.216]

Fulvestrant has been reported to decrease both insulin-like growth factor I (IGF-I) stimulated cell growth and IGF-I receptor mRNA (Huynh et al. 1996). Moreover, in the human fetal osteoblast cell line (hFOB/ER9 cells), both ICI 164384 and fulvestrant blocked the estradiol-induced increase in IGF-I mRNA levels (Kassem et al. 1998). [Pg.158]

Tumor necrosis factor a (TNF-a) is a multifunctional cytokine produced by activated monocytes-macrophages. TNF-a is one of the most potent osteoclastogenic cytokines produced in inflammation, and, in addition, TNF-a induces IL-1 synthesis. Like the other known stimulators of bone resorption, it acts through osteoblastic cells however, it has been demonstrated that TNF-a is able to induce osteoclast formation from stromal-depleted macrophages, with potency similar to that of RANKL (Kobayashi et al. 2000). TNF-a is able to induce bone resorption in vitro (Thomson et al. 1987) as well as in vivo (Koning et al. 1988). Osteoclasts induced by TNF-a have the capacity to form resorption pits on dentine slices only in the presence of IL-la. TNF-a, together with IL-1, plays an important role in bone resorption in inflammatory diseases (Kobayashi et al. 2000). Inhibition of TNF by TNF binding protein (TNFbp) completely prevents bone loss and osteoclast formation (Kimble et al. 1997). [Pg.176]

If the RANKL/OPG system is a final effector on the biology of osteoclasts, then this system should be the basis for the antiresorptive effects of estrogen. Indeed, estrogen stimulates OPG synthesis for osteoblastic cells (Hofbauer et al. 1999), estrogen deficiency induced by OVX results in a decrease in OPG and increased RANKL production, an action that is prevented by estradiol administration, and OPG administration prevents bone loss induced by OVX (Simonet et al. 1997 Hofbauer et al. 2000 Hofbauer 1999). In addition, estrogen can suppress RANKL and M-CSF-induced differentiation of myelomonocytic precursors into multinucleated TRAP+ osteoclasts through an ER-dependent mechanism that does not require mediation by stromal cells (Shevde et al. 2000). Finally, treatment with estradiol inhibits the response of osteoclast precursors to the action of RANKL (Srivastava et al. 2001). [Pg.183]

Thomson BM, Mundy GR, Chambers TJ (1987) Tumor necrosis factors alpha and beta induce osteoblastic cells to stimulate osteoclastic bone resorption. J Immunol 138 775-779... [Pg.189]

Hofbauer LC, Khosla S, Dunstan CR, Lacey DL, Spelsberg TC, Riggs BL (1999) Estrogen stimulates gene expression and protein production of osteoprotegerin in human osteoblastic cells. Endocrinology 140 4367-4370... [Pg.190]

Rickard DJ, Hofbauer LC, Bonde SK, Gori F, Spelsberg TC, Riggs BL (1998) Bone morphogenetic protein-6 production in human osteoblastic cell lines. Selective regulation by estrogen. J Clin Invest 101 413-422... [Pg.193]

Cheung J, Mak YT, Papaioannou S, Evans BA, Fogelman I, Hampson G (2003) Interleukin-6 (IL-6), IL-1, receptor activator of nuclear factor kappaB ligand (RANKL) and osteoprotegerin production by human osteoblastic cells comparison of the effects of 17-beta oestradiol and raloxifene. J Endocrinol 177 423-433... [Pg.194]

Nuttall ME, Stroup GB, Fisher PW, et al. (2000) Distinct mechanisms of action of selective estrogen receptor modulators in breast and osteoblastic cells. Am J Physiol Cell Physiol 279 C1550-C1557... [Pg.213]

Kozawa et al, 2000a and b). In both cell types, the p38 MAPK-specific inhibitor, SB203580, blocks SIP hsp27 induction and amplification of inositol phosphates, hi osteoblastic cells, PGE shmulates cyclic AMP formation and inhibits apoptosis. This appears to be mediated by a cyclic AMP-dependent modulation of SPHK and S IP production (Machwate etal., 1998)... [Pg.255]

Psseri G, Girasole G, Uloetti V, et al. Bisphosphonates inhibit IL-6 production by human osteoblastic cells MG-63. J Bone Min Res 1994 s230. [Pg.205]

Tintut Y, Parhami F, Le V, Karsenty G, and Demer LL (1999) Inhibition of osteoblast-specific transcription factor Cbfal by the cAMP pathway in osteoblastic cells. Ubiquitin/proteasome-dependent regulation. J. Biol. Chem. 274 28875-28879. [Pg.203]

Several excellent reviews on the biological role of fluoride have been published recently [79,175-176]. The main effect of fluoride is related to osteoblast cell proliferation. [Pg.319]

Fig. 11. Modes of action of fluorine on osteoblastic cells, (a) Tyrosine phosphatase hypothesis in osteoblastic cells, fluoride ion directly inhibits tyrosine phosphatase. Inhibition of this enzyme enhances the tyrosine phosphorylation of signalling molecules induced by receptor tyrosine kinase, which leads to activation of the extracellular signal-regulated kinase (ERK) through the Ras pathway and enhanced cell proliferation, (b) G-protein hypothesis in osteoblast-like cells, fluoride ions form a complex with aluminum, probably fluoroaluminate, which interacts with guanosine 5 -diphosphate (GDP) to form guanosine 5 -triphosphate (GTP)-like molecule. Activation of the G, protein stimulates the tyrosine phosphorylation of signalling molecules by a yet unknown tyrosine kinase (Tyr Kin) and activation of the ERK kinase through the Ras pathway leads to enhanced cell proliferation. (Reproduced by permission of Elsevier from Ref. [175] ... Fig. 11. Modes of action of fluorine on osteoblastic cells, (a) Tyrosine phosphatase hypothesis in osteoblastic cells, fluoride ion directly inhibits tyrosine phosphatase. Inhibition of this enzyme enhances the tyrosine phosphorylation of signalling molecules induced by receptor tyrosine kinase, which leads to activation of the extracellular signal-regulated kinase (ERK) through the Ras pathway and enhanced cell proliferation, (b) G-protein hypothesis in osteoblast-like cells, fluoride ions form a complex with aluminum, probably fluoroaluminate, which interacts with guanosine 5 -diphosphate (GDP) to form guanosine 5 -triphosphate (GTP)-like molecule. Activation of the G, protein stimulates the tyrosine phosphorylation of signalling molecules by a yet unknown tyrosine kinase (Tyr Kin) and activation of the ERK kinase through the Ras pathway leads to enhanced cell proliferation. (Reproduced by permission of Elsevier from Ref. [175] ...
The data concerning the effect of fluoride-containing apatites on cell adhesion, proliferation and expression seem rather disparate, probably because of the variation of other surface characteristics and the use of different cell strains. No real negative effect of fluoride-containing substrates has been reported so far and the osteoblast cells seem to behave similarly [184,185] or better [183,186,187] on fluoridated apatites than on HA surfaces. Some reports mention weaker attachment and proliferation, compensated for by improved collagen matrix production [188]. The shape of cells appeared different on fluoridated apatites than on HA. Other authors have found an improvement in cell attachment [183] which has been attributed to the change in surface charge of FA compared to HA. [Pg.321]

A.S. Santiago, E.A. Santos, M.S. Sader, M.F. Santiago, G.A. Soares, Response of osteoblastic cells to titanium submitted to three different surface treatments, Pesqui. Odont. Bras. 19 (2005) 203-208. [Pg.331]

Chang, E-J. et al.. Proliferative effects of fiavan-3-ols and propelargonidins from rhizomes of Drynaria fortunei on MCF-7 and osteoblastic cells. Arch. Pharm. Res., 26, 620, 2003. [Pg.611]

Abundant data indicate that Ca + inhibits the formation and activity of osteoclasts and stimulates the activity of osteoblasts. The first evidence for the existence of a G protein-coupled, cation-sensing mechanism in osteoblasts was presented shortly after the cloning of the CaR (Quarles et al, 1994). Since then some, but not all studies have found that the CaR is expressed in various osteoblastic cell lines and primary osteoblasts (Chang et al, 1999 Chattopadhyay et al, 2004 ... [Pg.148]

Bradford PG, Maglich JM, Kirkwood KL. 2000. IL-1 (3 increases type 1 inositol trisphosphate receptor expression and IL-6 secretory capacity in osteoblastic cell cultures. Mol Cell Biol Res Commun 3 73-5. [Pg.555]

Civitelli R, Beyer EC, Warlow PM, Robertson AJ, Geist ST, Steinberg TH. 1993. Connexin43 mediates direct intercellular communication in human osteoblastic cell networks. J. Clin. Invest 91 1888-1896. [Pg.555]

Gofa A, Davidson RM. 1996. NaF potentiates a K+-selective ion channel in G292 osteoblastic cells. J Membr Biol 149 211-9. [Pg.556]

Jorgensen NR, Teilmann SC, Henriksen Z, Civitelli R, Sorensen OH, Steinberg TH. 2003. Activation of L-type calcium channels is required for gap junction-mediated intercellular calcium signaling in osteoblastic cells. J Biol Chem 278 4082—6. [Pg.557]

Romanello M, Padoan M, Franco L, Veronesi V, Moro L, D Andrea P. 2001. Extracellular NAD+ induces calcium signaling and apoptosis in human osteoblastic cells. Biochem Biophys Res Commun 285 1226-31. [Pg.559]


See other pages where Osteoblast cells is mentioned: [Pg.222]    [Pg.121]    [Pg.197]    [Pg.99]    [Pg.100]    [Pg.121]    [Pg.38]    [Pg.10]    [Pg.311]    [Pg.166]    [Pg.189]    [Pg.299]    [Pg.195]    [Pg.116]    [Pg.181]    [Pg.280]    [Pg.321]    [Pg.322]    [Pg.271]    [Pg.269]    [Pg.165]   
See also in sourсe #XX -- [ Pg.321 ]




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