Long-term anabolic effects of prostaglandin-E2 on tibial diaphyseal bone in male rats

Jee, Webster S. S.; Ke, Hua Zhu; Li, Xiao Jian

doi:10.1016/0169-6009(91)90109-d

Cited by 86 publications

(37 citation statements)

References 22 publications

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“…Under both conditions, either exogenous S1P was added or components of the signaling pathway (i.e., Sphk1 or the S1P 2 receptor) were inhibited. The cellular responses determined comprised intracellular Ca 2+ (immediate response) [25], prostaglandin E2 (PGE 2 ) release [27,28] and mRNA (COX-2 gene) expression (intermediate response) [28][29][30] and receptor activator of nuclear factor kappa B (NF-κB) ligand (RANKL) and osteoprotegerin (OPG) mRNA expression (late-stage response) [9,[31][32][33].…”

Section: Introductionmentioning

confidence: 99%

The role of the sphingosine-1-phosphate signaling pathway in osteocyte mechanotransduction

Zhang

Zhao

Liu

et al. 2015

Bone

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Section: Introductionmentioning

confidence: 99%

The role of the sphingosine-1-phosphate signaling pathway in osteocyte mechanotransduction

Zhang

Zhao

Liu

et al. 2015

Bone

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“…Prostaglandins are potent stimulators of bone resorption in organ culture (Dietrich et al, 1975) but inhibit bone resorption by isolated osteoclasts (Fuller and Chambers, 1989). They can also both stimulate and inhibit bone formation (Ffaisz and Fall, 1990;Jee et al, 1991). Prostaglandins play a role in bone loss due to inflammation and immobilization (Thompson and Rodan, 1988) and are produced by isolated bone cells in response to mechanical stress (Burger and Veldhuijzen, 1993).…”

mentioning

confidence: 97%

Prostaglandin mediated modulation of transforming growth factor-β metabolism in primary mouse osteoblastic cells in vitro

1996

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Prostaglandins and transforming growth factor-beta (TGF-beta) are both important local regulators of bone metabolism, but their actions on bone are complex. Prostaglandins mediate bone loss due to immobilization, but prostaglandin E2 (PGE2) treatment stimulates bone formation in vivo. TGF-beta may have both anabolic and catabolic effects on bone in vitro. In this study, we tested the effects of PGE2 on TGF-beta release and on TGF-beta messenger RNA (mRNA) levels in neonatal mouse calvarial cell cultures. We also examined the relationship between endogenous prostaglandin production as a result of mechanical stress and the release of TGF-beta. Addition of PGE2 (10(-8)-10(-6)M) to the culture medium stimulated the release of TGF-beta peptide (active plus latent) after 24 and 48 h in a dose-related manner. This upregulation was paralleled by an increased expression of TGF-beta mRNA levels. Mechanical stimulation by 1 h treatment with pulsating fluid flow (producing a shear stress of 0.5 +/- 0.02 Pa at 5 Hz) resulted 1 h posttreatment in increased production of PGE2, prostaglandin l2 (PGI2), and prostaglandin F2a. In addition, the release of TGF-beta activity but not TGF-beta peptide was decreased 24 h after PFF treatment. Addition of indomethacin, which blocks endogenous prostaglandin production, neutralized the effect of PFF treatment on TGF-beta activity, indicating that the effect of stress was mediated by endogenous prostaglandins. These results suggest that PGE2 and other prostaglandins (probably PGI2 and/or PGF2a) have opposite effects on TGF-beta metabolism in bone cells, as PGE2 upregulates TGF-beta expression and synthesis while other prostaglandins downregulate TGF-beta activation.

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“…Substantial research efforts in this area have been focused on effective incorporation of synergistic growth factors, such as bone morphogenetic proteins (BMPs), into the bone grafts [1][2][3]. Compared to these biologics, the clinical applications of low molecular weight bone anabolic agents such as prostaglandins (E 1 and E 2 ) [4,5], statins [6] and prostaglandin EP 4 receptor agonists [7,8] have not yet been developed. Prostaglandins are locally secreted, rapidly metabolized, biologically active fatty acids first identified in the prostate [9].…”

Section: Introductionmentioning

confidence: 99%

Osteotropic β-cyclodextrin for local bone regeneration

Liu¹,

Wiswall²,

Rutledge³

et al. 2008

Biomaterials

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An osteotropic alendronate-β-cyclodextrin conjugate (ALN-β-CD) was developed as a bonetargeting delivery system for improved treatment of skeletal diseases. The conjugate shows very strong binding to hydroxyapatite (HA, main component of the skeleton). Its ability in forming molecular inclusion complex with prostaglandins E 1 (PGE 1 , a potent bone anabolic agent) was confirmed by phase-solubility experiments and differential scanning calorimetry (DSC). In a bilateral rat mandible model, ALN-β-CD/PGE 1 molecular complex was shown to stimulate strong local bone anabolic reaction. In the control study, ALN-β-CD itself was also found to be bone anabolic. To investigate this finding, other control groups were studied. The histomorphometry data suggests that ALN-β-CD itself could generate more new bone at the injection site than its complex with PGE 1 . Alendronate (ALN) injection could also cause new bone formation, which locates peripheral to the site of injection. PGE 1 , saline or ethanol injections do not have anabolic effect. These findings were also confirmed by micro-CT evaluation of mandibular bones. It is clear that the bone anabolic effect of ALN-β-CD is independent of mechanical stimuli of the periosteum or ALN injection alone. Further studies are warranted to understand the working mechanism of ALN-β-CD as a bone anabolic agent.

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Long-term anabolic effects of prostaglandin-E2 on tibial diaphyseal bone in male rats

Cited by 86 publications

References 22 publications

The role of the sphingosine-1-phosphate signaling pathway in osteocyte mechanotransduction

The role of the sphingosine-1-phosphate signaling pathway in osteocyte mechanotransduction

Prostaglandin mediated modulation of transforming growth factor-β metabolism in primary mouse osteoblastic cells in vitro

Osteotropic β-cyclodextrin for local bone regeneration

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