scholarly journals High-phosphorus diet stimulates receptor activator of nuclear factor-κB ligand mRNA expression by increasing parathyroid hormone secretion in rats

2005 ◽  
Vol 94 (5) ◽  
pp. 666-674 ◽  
Author(s):  
Shin-ichi Katsumata ◽  
Ritsuko Masuyama ◽  
Mariko Uehara ◽  
Kazuharu Suzuki
Keyword(s):  
Parathyroid Hormone ◽  
Bone Loss ◽  
Mrna Expression ◽  
Bone Mineral ◽  
Lumbar Vertebra ◽  
The Other ◽  
Osteoclast Number ◽  
Rankl Mrna ◽  
Receptor Activator ◽  
Rankl Mrna Expression

The purpose of the present study was to clarify the manner by which the supplementation of high-P diet induces bone loss. Eighteen 4-week-old male Wistar-strain rats were assigned randomly to three groups and fed diets containing three P levels (0·3, 0·9, and 1·5%) for 21d. A lower serum Ca concentration was observed in the rats fed on the 1·5% P diet than in the other two groups. Serum P and parathyroid hormone concentrations and urinary excretion of C-terminal telopeptide of type I collagen were elevated with increasing dietary P levels. Serum osteocalcin concentration was increased in the rats fed on the 1·5% P diet than in the other two groups. Bone formation rate of the lumbar vertebra was significantly increased in the two high-P groups than in the 0·3% P group. Osteoclast number was significantly increased with increasing dietary P levels. Bone mineral content and bone mineral density of the femur and lumbar vertebra and ultimate compression load of the lumbar vertebra were decreased with increasing dietary P levels. Additionally, ultimate bending load of the femur was decreased in the rats fed on the 1·5% P diet than in the other two groups. Receptor activator of NF-κB ligand (RANKL) mRNA expression in the femur was significantly higher with increasing dietary P levels. These results suggest that secondary hyperparathyroidism due to a high-P diet leads to bone loss via an increase in bone turnover. Furthermore, an increase in osteoclast number was caused by increased RANKL mRNA expression.

scholarly journals Genistein modulates the effects of parathyroid hormone in human osteoblastic SaOS-2 cells

2006 ◽  
Vol 95 (6) ◽  
pp. 1039-1047 ◽  
Author(s):  
Wen-Fang Chen ◽  
Man-Sau Wong
Keyword(s):  
Parathyroid Hormone ◽  
Mrna Expression ◽  
Osteoblastic Cells ◽  
Dependent Manner ◽  
Alp Activity ◽  
Rankl Mrna ◽  
Receptor Activator ◽  
Pre Treatment ◽  
Dose Dependent ◽  
Rankl Mrna Expression

Genistein and parathyroid hormone (PTH) are anabolic agents that stimulate bone formation through their direct actions in osteoblastic cells. In the present study, we aimed to determinewhether genistein modulates the actions of PTH in human osteoblastic SaOS-2 cells in an oestrogen-depleted condition. The present results showed that genistein (10−8to 10−6m) induced alkaline phosphatase (ALP) activity and osteoprotegrin (OPG) expression in SaOS-2 cells in a dose-dependent manner. These effects could be completely abolished by co-treatment with oestrogen antagonist ICI 182780 (7α-[9-[(4,4,5,5,5-pentafluoropentyl)sulfonyl]nonyl]-estra-1,3,5(10)-triene-3,17β-diol). Genistein (at 1μm) could stimulate the mRNA expression of receptor activator of NF-κB ligand (RANKL). As OPG and RANKL are known to modulate osteoclastogenesis, the ability of genistein to modulate OPG and RANKL expression in SaOS-2 cells suggested that it might modulate osteoclastogenesis through its direct actions on osteoblastic cells. PTH (at 10nm) stimulated ALP activity, induced RANKL mRNA expression and suppressed OPG mRNA expression in SaOS-2 cells, confirming its bi-directional effects on osteoblastic cells. Pre-treatment of SaOS-2 cells with genistein andoestrogen not only enhanced PTH-induced ALP activity, but also attenuated PTH up regulation ofRANKL mRNA expression and PTH down regulation of OPG mRNA expression. Taken together, the present study provides the first evidence that genistein could modulate the actions of PTH in human osteoblastic SaOS-2 cells in an oestrogen-depleted condition.

scholarly journals Effects of ginsenoside Rg3 on bone loss, bone mineral density and osteoclast number in glucocorticoid-induced osteoporosis rats, and the likely michanism of action

2020 ◽  
Vol 19 (4) ◽  
pp. 811-815
Author(s):  
Maoxiu Peng ◽  
Gangyl Jiang ◽  
Shaoqi He ◽  
Chengxuan Tang
Keyword(s):  
Bone Mineral Density ◽  
Bone Loss ◽  
Bone Mineral ◽  
Lumbar Vertebrae ◽  
Ginsenoside Rg3 ◽  
Model Group ◽  
Mineral Density ◽  
Alendronate Sodium ◽  
Trabecular Thickness ◽  
Osteoclast Number

Purpose: To investigate the effect of ginsenoside Rg3 on bone loss, bone mineral density (BMD) and osteoclast number in glucocorticoid-induced osteoporosis (GIOP) rats, and the mechanism of action involved.Methods: Sixty female Wistar rats were assigned to control, model group, ginsenoside Rg3, and alendronate sodium groups, comprised of 15 rats per group. The osteoporosis rat model was established via intramuscular injection of dexamethasone. Changes in bone mineral content (BMC), BMD trabecular thickness and area, osteoblasts and osteoclasts in femurs and lumbar vertebrae were measured after 3 months of treatment.Results: There were significantly higher BMC and BMD levels in ginsenoside Rg3 group than in alendronate rats (p < 0.05). The thickness and  trabecular area in femur and lumbar vertebrae in the ginsenoside Rg3 group were significantly higher than those in the model group (p < 0.05), but were comparable with those in the alendronate sodium group (p > 0.05). There were marked increases in osteoblasts, and marked decreases in osteoclasts in the ginsenoside Rg3 group, alendronate sodium and control rats, relative to model rats (p < 0.05).Conclusion: Ginsenoside Rg3 arrests bone loss, and enhances bone density, trabecular thickness and area, bone microstructure, osteoblast activity and population of osteoclasts number in glucocorticoidinduced osteoporotic rats. This provides a new research direction for the clinical treatment ofosteoporosis. Keywords: Ginseng soap, Rg3, Glucocorticoid, Osteoporosis, Bone loss, Bone mineral density, Osteoclast population

IL-6 is not required for parathyroid hormone stimulation of RANKL expression, osteoclast formation, and bone loss in mice

2005 ◽  
Vol 289 (5) ◽  
pp. E784-E793 ◽  
Author(s):  
Charles A. O'Brien ◽  
Robert L. Jilka ◽  
Qiang Fu ◽  
Scott Stewart ◽  
Robert S. Weinstein ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Bone Loss ◽  
Secondary Hyperparathyroidism ◽  
Osteoclast Formation ◽  
Luciferase Reporter ◽  
Wild Type ◽  
Deficient Diet ◽  
Rankl Mrna ◽  
Deficient Mice

Continuous elevation of parathyroid hormone (PTH) increases osteoclast precursors, the number of osteoclasts on cancellous bone, and bone turnover. The essential molecular mediators of these effects are controversial, however, and both increased receptor activator of NF-κB ligand (RANKL) and IL-6 have been implicated. The goal of these studies was to determine whether continuous elevation of endogenous PTH alters IL-6 gene expression in vivo and whether IL-6 is required for PTH-induced bone loss. To accomplish this, we generated transgenic mice harboring a luciferase reporter gene under the control of IL-6 gene regulatory regions to allow accurate quantification of IL-6 gene activity in vivo. In these mice, induction of secondary hyperparathyroidism using a calcium-deficient diet did not alter IL-6-luciferase transgene expression, whereas RANKL mRNA expression was elevated in bone tissue. Moreover, secondary hyperparathyroidism induced an equivalent amount of bone loss in wild-type and IL-6-deficient mice, and PTH elevated RANKL mRNA and osteoclast formation to the same extent in bone marrow cultures derived from wild-type and IL-6-deficient mice. These results demonstrate that IL-6 is not required for the osteoclast formation and bone loss that accompanies continuous elevation of PTH.

Osteoclast and Osteoblast Activities on Carbonate Apatite Plates in Cell Cultures

2010 ◽  
Vol 26 (4) ◽  
pp. 435-449 ◽  
Author(s):  
Keiichi Kanayama ◽  
Wantida Sriarj ◽  
Hitoyata Shimokawa ◽  
Keiichi Ohya ◽  
Yutaka Doi ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Bone Marrow Cells ◽  
Cathepsin K ◽  
The Other ◽  
Mouse Bone Marrow ◽  
Carbonate Apatite ◽  
Icr Mouse ◽  
Rankl Mrna ◽  
Osteoclastic Resorption ◽  
Mouse Osteoblast

Previous studies have demonstrated that carbonate apatite (CA) is superior to hydroxyapatite (HA) and β-tricalciumphosphate (β-TCP) with regard to osteoclastic resorption, but evidence on osteoclast and osteoblast response remains controversial. In the present study, the expression of bone related mRNA is examined on CA, HA, β-TCP, and titanium plates. ICR mouse osteoblast cells are cocultured with ICR mouse bone marrow cells. Crude osteoclast-like cell-rich suspensions are then seeded onto plates and cultured for 48 h. Total RNA is extracted and mRNA expression is examined by real-time RT-PCR. Amounts of vacuolar-type ATPase, cathepsin K, and TRAP mRNA are significantly greater on CA than on the other plates. The amount of osteoprotegerin mRNA is significantly greater on CA than on the other plates. RANKL mRNA expression, which is generally regarded as an osteoblast maker, varies with material, but shows no significant differences between CA and the other plates. The formation and activity of osteoclasts is greater with CA than with the other plates. Thus, CA is superior to β-TCP as a bioresorbable bone substitute for tissue engineering.

scholarly journals INTERLEUKIN-8 RELATED WITH BONE MINERAL DENSITY (Interleukin-8 terkait Kepadatan Mineral Tulang)

2018 ◽  
Vol 22 (3) ◽  
pp. 237
Author(s):  
Yurdiansyah Latif ◽  
Uleng Bahrun ◽  
Ruland Pakasi
Keyword(s):  
Bone Mineral Density ◽  
Bone Mineral ◽  
Interleukin 8 ◽  
Mineral Density ◽  
Rankl Mrna ◽  
Receptor Activator ◽  
Nf Kappab

Osteoporosis merupakan salah satu penyebab cacat pada usia lanjut karena kebahayaan patah tulang yang disebabkannya. Mulaiusia 50 tahun kemungkinan mengalami patah tulang bagi perempuan adalah 40%‚ sedangkan bagi laki-laki 13%. Angka prevalensiosteopeni di Indonesia sebesar 41‚7% dan osteoporosis sebesar 10‚3%. Hal ini berarti dua dari lima penduduk memiliki kebahayaan untukterkena osteoporosis. Interleukin-8 diduga berperan dalam merangsang pembuatan Receptor Activator of NF KappaB Ligand (RANKL)mRNA di osteoblast yang mengikat reseptor RANK di osteoklast yang berperan dalam penurunan kepadatan mineral tulang. Kajianini bertujuan untuk mengetahui kadar Interleukin-8 dan hubungannya dengan kepadatan mineral tulang yang normal, osteopeniadan osteoporosis secara penentuan. Penelitian dilakukan secara potong lintang selama masa waktu antara bulan Mei 2012−Mei 2013menggunakan data primer pemeriksaan kadar Interleukin-8 dan kepadatan mineral tulang pada perempuan yang berusia antara 30−60tahun di Makassar. Data dianalisis dan diolah dengan uji Anova. Kadar interleukin-8 lebih tinggi di densitas mineral tulang (DMT)osteoporosis dibandingkan dengan DMT yang normal dan osteopenia dengan kadar IL-8 pada DMT normal 48,72±12,81, osteopenia55,68±13,75, osteoporosis 62,06±24,45. Hubungan antara IL-8 pada perempuan dengan DMT yang normal dibandingkan denganosteoporosis memperoleh nilai p=0,03, perempuan dengan DMT normal dengan osteopenia p=0,51 dan perempuan osteopenia denganosteoporosis p=0,62. Didasari telitian ini, dapat disimpulkan bahwa terdapat hubungan bermakna antara peningkatan kadar IL-8dengan kepadatan mineral tulang yang berkurang di kelompok perempuan osteoporosis dibandingkan dengan kelompok DMT yangnormal. Para peneliti berpendapat untuk meneliti lanjutan dengan memperhatikan ciri indeks masa tubuh di sampel penelitian.

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