Prostaglandin E2 prevents bone loss and adds extra bone to immobilized distal femoral metaphysis in female rats

Akamine, Takuya; Jee, Webster S. S.; Ke, Hua Zhu; Li, X.J.; Lin, Bai Yun

doi:10.1016/8756-3282(92)90356-2

Cited by 93 publications

(30 citation statements)

References 21 publications

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“…Among the bone-modeling cells, PGE2 is produced mainly by osteoblasts 56,57 and has been reported to enhance bone formation at low doses but increase bone resorption at high doses. [2][3][4][5][6] The differential effects of PGE2 are attributed to the presence of multiple cell-surface PG receptors. 58 -63 Systemic or local injections of PGE2 have also been shown to stimulate bone formation in rats 2,62 and in piglets, 55 and reduce bone loss in rats attributable to disuse or orchidectomy.…”

Section: Discussionmentioning

confidence: 99%

“…1 In contrast, prostaglandins (PGs), eg, PGE 2 , derived from COX metabolism of AA enhance bone formation and mass by increasing osteoblast replication and differentiation and/or by inhibiting osteoclastic resorption, [2][3][4][5] …”

mentioning

confidence: 99%

“…The 5-LO products leukotrienes and 5-HETE (hydroxyeicosatetraenoic acid) function as negative modulators of bone formation by inhibiting osteoblast differentiation and bone formation. 1 In contrast, prostaglandins (PGs), eg, PGE 2 , derived from COX metabolism of AA enhance bone formation and mass by increasing osteoblast replication and differentiation and/or by inhibiting osteoclastic resorption, [2][3][4][5] although high concentrations of PGE 2 can stimulate bone resorption. 6 Dietary supplementation with AA results in increases in bone mass and volume, 7,8 reflecting a beneficial role of eicosanoids in bone formation.…”

mentioning

confidence: 99%

“…Because adipocytes and osteoblasts share a common mesenchymal stem cell origin, our findings suggest that absence of iPLA 2 Bioactive arachidonic acid (AA) metabolites (eicosanoids) generated by the actions of various oxygenases, such as the 5-lipoxygenase (5-LO) and cyclooxygenase (COX) isozymes, are important mediators of bone remodeling. The 5-LO products leukotrienes and 5-HETE (hydroxyeicosatetraenoic acid) function as negative modulators of bone formation by inhibiting osteoblast differentiation and bone formation.1 In contrast, prostaglandins (PGs), eg, PGE 2 , derived from COX metabolism of AA enhance bone formation and mass by increasing osteoblast replication and differentiation and/or by inhibiting osteoclastic resorption, [2][3][4][5] …”

mentioning

confidence: 99%

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Age-Related Changes in Bone Morphology Are Accelerated in Group VIA Phospholipase A2 (iPLA2β)-Null Mice

Ramanadham

Yarasheski

Silva

et al. 2008

The American Journal of Pathology

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Phospholipases A 2 (PLA 2 ) hydrolyze the sn؊2 fatty acid substituent, such as arachidonic acid, from phospholipids, and arachidonate metabolites are recognized mediators of bone modeling. We have previously generated knockout (KO) mice lacking the group VIA PLA 2 (iPLA 2 ␤), which participates in a variety of signaling events; iPLA 2 ␤ mRNA is expressed in bones of wild-type (WT) but not KO mice. Cortical bone size, trabecular bone volume, bone mineralizing surfaces, and bone strength are similar in WT and KO mice at 3 months and decline with age in both groups, but the decreases are more pronounced in KO mice. The lower bone mass phenotype observed in KO mice is not associated with an increase in osteoclast abundance/activity or a decrease in osteoblast density, but is accompanied by an increase in bone marrow fat. Relative to WT mice, undifferentiated bone marrow stromal cells (BMSCs) from KO mice express higher levels of PPAR-␥ and lower levels of Runx2 mRNA, and this correlates with increased adipogenesis and decreased osteogenesis in BMSCs from these mice. In summary, our studies indicate that age-related losses in bone mass and strength are accelerated in iPLA 2 ␤-null mice. Because adipocytes and osteoblasts share a common mesenchymal stem cell origin, our findings suggest that absence of iPLA 2 Bioactive arachidonic acid (AA) metabolites (eicosanoids) generated by the actions of various oxygenases, such as the 5-lipoxygenase (5-LO) and cyclooxygenase (COX) isozymes, are important mediators of bone remodeling. The 5-LO products leukotrienes and 5-HETE (hydroxyeicosatetraenoic acid) function as negative modulators of bone formation by inhibiting osteoblast differentiation and bone formation.1 In contrast, prostaglandins (PGs), eg, PGE 2 , derived from COX metabolism of AA enhance bone formation and mass by increasing osteoblast replication and differentiation and/or by inhibiting osteoclastic resorption, [2][3][4][5]

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Age-Related Changes in Bone Morphology Are Accelerated in Group VIA Phospholipase A2 (iPLA2β)-Null Mice

Ramanadham

Yarasheski

Silva

et al. 2008

The American Journal of Pathology

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“…Particularly as local delivery of prostaglandin E1 (PGE1) has been shown to enhance the formation of mandibular alveolar bone, reorganization of adjacent cells in the periodontal ligament and cementum formation [11,13,18]. The positive effect of PGE 2 on bone deposition has been reported with doses as low as 1 mg/kg per day delivered subcutaneously into different animal models over extended periods of time [1,6,9,20]. In load-bearing bones, PGE 2 has an anabolic effect when administered either systemically or locally [7].…”

Section: Introductionmentioning

confidence: 99%

Prostaglandin E2 enhances alveolar bone formation in the rat mandible

Ramirez-Yañez

Seymour

Walsh

et al. 2004

Bone

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Prostaglandin E 2 (PGE 2 ) induces bone formation in stress-bearing bones. The mandible, a stress-bearing bone, is loaded daily during mastication. The aim of this study was to determine if PGE 2 delivered locally to the mandible over 20 days enhances alveolar bone deposition. In 18 Lewis rats, controlled-release pellets containing PGE 2 were implanted on the buccal aspect on the left-hand side of the mandible, mesial to the root of the first molar. Controlled-release pellets locally delivered 0.1, 0.05, or 0.025 mg/day of PGE 2 . The right side of the mandible was used as a matched control for each animal. Six sham-treated animals were implanted with a placebo pellet. On days 7 and 19, animals were injected with the bone markers tetracycline and calcein, respectively. On day 21, animals were sacrificed and undecalcified tissues obtained for morphometrical analysis. Morphometrical measurements were analyzed by paired t test to determine differences between the matched samples and one-way ANOVA to compare the different treatment groups. A significant increase in alveolar bone area was observed in mandibles treated with 0.1 and 0.05 mg/day when compared with matched controls and the placebo group. This was accompanied by a significant increase in alveolar bone height and width. The proportions of double-labeled surface (dLS), the mineral apposition rate (MAR), and bone formation rate (BFR) were significantly increased in mandibles treated with the two higher doses of PGE 2 . The proportion of resorptive surface (RS) was significantly reduced in these two groups. It is concluded that PGE 2 induces alveolar bone formation in the mandible when locally delivered at a dose of 0.1 or 0.05 mg/day for 20 days.

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Functional characterization of prostaglandin E2 inducible osteogenic colony forming units in cultures of cells isolated from the neonatal rat calvarium

et al. 1996

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Prostaglandin E2 (PGE2) increases the number of mineralized nodules that form in cultures of rat calvarial (RC) cells. The purpose of our study was to characterize PGE2-inducible osteogenic colony forming units (CFU-Os) by determining their number, the cell populations from which they were released, their specific responsive period to PGE2, and their proliferating and differentiating characteristics under the stimulation of PGE2. Limiting dilution analysis was used to determine the number of PGE2-inducible CFU-Os. Sequential digestion of intact rat parietal bones with collagenase isolated 5 subpopulations of RC cells that were used to estimate the cell populations where PGE2-inducible CFU-Os resided. The responsive period of PGE2-inducible CFU-Os to PGE2 was evaluated by treating cultures of mixed RC cells for all possible combinations of days 1-10, 11-20, and 21-30. PGE2 effects on proliferation and differentiation of CFU-Os were evaluated by comparing the DNA synthesis and AP activity in subpopulations I and IV on days 3, 6, and 9. Results showed: (1) PGE2-inducible CFU-Os represent 0.27% of cells in the mixed RC population, (2) the majority of determined and PGE2-inducible CFU-Os were found in the subpopulations released during the 60-100 min digestion periods, (3) the response of PGE2-inducible CFU-Os is limited to the first 10 days of culture, and (4) PGE2-stimulated nodule formation is associated with an early increase in DNA synthesis and a sustained increase in alkaline phosphatase activity. We conclude that, functionally, PGE2-inducible CFU-Os are slowly proliferating AP negative cells primarily found in the subpopulations III-V. PGE2 stimulates them to proliferate and become AP+, and function as determined CFU-Os to form mineralized nodules in vitro.

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Prostaglandin E2 prevents bone loss and adds extra bone to immobilized distal femoral metaphysis in female rats

Cited by 93 publications

References 21 publications

Age-Related Changes in Bone Morphology Are Accelerated in Group VIA Phospholipase A2 (iPLA2β)-Null Mice

Age-Related Changes in Bone Morphology Are Accelerated in Group VIA Phospholipase A2 (iPLA2β)-Null Mice

Prostaglandin E2 enhances alveolar bone formation in the rat mandible

Functional characterization of prostaglandin E2 inducible osteogenic colony forming units in cultures of cells isolated from the neonatal rat calvarium

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