Histamine stimulates production of osteoclast differentiation factor/receptor activator of nuclear factor-κB ligand by osteoblasts

Deyama, Yoshiaki; Kikuiri, Takashi; Ohnishi, Gen ichi; Feng, Yi; Takeyama, Sadaaki; Hatta, Mitsutoki; Yoshimura, Yoshitaka; Suzuki, Kuniaki

doi:10.1016/s0006-291x(02)02440-3

Cited by 39 publications

(29 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this study, using primary osteoblasts we found that histamine targets osteoblasts and modulates RANKL/OPG ratio and confirmed that RANKL was up-regulated 14,15 ; in contrast, OPG expression was not affected by histamine, so that RANKL/OPG ratio shifted in favor of osteoclastogenesis. By locally secreting histamine, osteoclast precursors probably induce an increase in RANKL/OPG ratio by the osteoblasts, which in turn enhances osteoclast differentiation and activity, thus providing a rare example of communication in this direction.…”

Section: Discussionsupporting

confidence: 73%

“…8,9 Biopsies from patients with systemic mastocytosis shows evidence of increased cortical and trabecular bone turnover in regions of mast cell accumulation. 31 Using other in vitro models (bone marrow cells or co-culture of osteoblasts and bone marrow), previous studies already showed that histamine promotes osteoclast differentiation 12,13,14,15 and it was suggested that this effect of histamine could be explained by the increased RANKL expression in osteoblasts.…”

Section: Discussionmentioning

confidence: 99%

“…13 It was shown in vitro, in bone marrow cultures or co-cultures, that histamine can increase osteoclast differentiation and that H1R and H2R antagonists partially inhibit histamine increase. 12,14,15 Also, it was demonstrated that osteoblasts express H1R and H2R and that histamine increase RANKL expression in these cells. 14,15 In this study, we focused on the osteoclast and the osteoclast precursors, and looked for a direct action of histamine on these cells, using in vivo and in vitro approaches.…”

mentioning

confidence: 99%

“…12,14,15 Also, it was demonstrated that osteoblasts express H1R and H2R and that histamine increase RANKL expression in these cells. 14,15 In this study, we focused on the osteoclast and the osteoclast precursors, and looked for a direct action of histamine on these cells, using in vivo and in vitro approaches. We assessed the effects of histamine deficiency and increase, and specific inhibition of histamine receptors on osteoclast differentiation and activity, and determined the histamine receptors implicated.…”

mentioning

confidence: 99%

See 3 more Smart Citations

Histamine Promotes Osteoclastogenesis through the Differential Expression of Histamine Receptors on Osteoclasts and Osteoblasts

Duplan

Baroukh

et al. 2009

The American Journal of Pathology

View full text Add to dashboard Cite

In addition to the numerous roles of histamine in both the immune and nervous systems, previous studies have suggested that this bioamine might also be involved in bone metabolism. Following our observations of impaired bone resorption in ovariectomized rats after histamine receptor antagonist treatment, we focused in this study on osteoclasts and osteoclast precursors. We looked for a direct action of histamine on these cells using both in vivo and in vitro approaches. In vivo, we triggered a remodeling sequence in rat mandibular bone and treated the animals with either histamine or histamine receptor antagonists. Histamine was shown to increase the number of osteoclasts and osteoclast precursors whereas antagonists of histamine receptor-1 and -2 decreased both osteoclast recruitment and resorption. In vitro, spleen cells from histamine-deficient mice were treated with receptor activator for nuclear factor kappa B ligand and macrophage colony stimulating factor, giving rise to both reduced numbers of osteoclasts and decreased resorption on dentin slices. Histamine enhanced resorption in these cultures in a dose-dependent manner. In addition, we identified osteoclast precursors as a source of histamine. In contrast, histamine increased the receptor activator for nuclear factor kappa B ligand/osteoprotegerin ratio in primary osteoblasts that did not secrete histamine. We observed a differential expression of histamine receptor-1 and -2 mRNAs in both primary osteoclasts and osteoblasts, confirming their functional roles with selective antagonists. Thus, histamine acts directly on osteoclasts, osteoclast precursors, and osteoblasts, promoting osteoclastogenesis through autocrine/paracrine mechanisms.

show abstract

Section: Discussionsupporting

confidence: 73%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Histamine Promotes Osteoclastogenesis through the Differential Expression of Histamine Receptors on Osteoclasts and Osteoblasts

Duplan

Baroukh

et al. 2009

The American Journal of Pathology

View full text Add to dashboard Cite

show abstract

“…These cells are tightly regulated by systemic or local factors, such as RANKL, which is generated by osteoblasts and bone marrow stromal cells in response to various stimuli, including vitamin D 3 , parathyroid hormone, TNF-␣, thyroid hormone, lipopolysaccaride, IL-1, IL-11, histamine, fibroblast growth factor-2, insulin-like growth factor-1, and CpGpDNA (3)(4)(5)(6)(7)(8)(9).…”

mentioning

confidence: 99%

μ-Calpain Regulates Receptor Activator of NF-κB Ligand (RANKL)-supported Osteoclastogenesis via NF-κB Activation in RAW 264.7 Cells

Lee

Kim

Karmin

et al. 2005

Journal of Biological Chemistry

View full text Add to dashboard Cite

To clarify the role of calpain in the receptor activator of NF-B ligand (RANKL)-supported osteoclastogenesis, RANKL-induced calpain activation was examined by using murine RAW 264.7 cells and bone marrow-derived monocyte/macrophage progenitors. We found that calpain activity increased in response to RANKL in both cell types based on ␣-spectrinolysis and that -calpain, rather than m-calpain, was activated during RANKLsupported osteoclastogenesis in RAW 264.7 cells. Overexpression of -calpain clearly augmented RANKL-supported osteoclastogenesis in RAW 264.7 cells, thereby implicating its pivotal role in this process. Cell-permeable calpain inhibitors, including calpastatin and calpeptin, were sufficient to suppress RANKL-supported osteoclastogenesis based on decreased expression of the osteoclastogenic marker, matrix metalloproteinase 9, and the generation of tartrate-resistant acid phosphatase-positive multinucleated cells in both cell types. Calpain inhibitors suppressed NF-B activation via inhibition of the cleavage of inhibitor of NF-B (IB␣) in RAW 264.7 cells. Taken together, our findings suggest that -calpain is essential to the regulation of RANKL-supported osteoclastogenesis via NF-B activation.

show abstract

Effects of the Histamine 1 Receptor Antagonist Cetirizine on the Osteoporotic Phenotype in H⁺/K⁺ATPase Beta Subunit KO Mice

Aasarød¹,

Stunes²,

Mosti³

et al. 2016

J of Cellular Biochemistry

View full text Add to dashboard Cite

Epidemiological studies suggest increased fracture risk in patients using proton pump inhibitors (PPIs). We have previously shown that the H(+) /K(+) ATPase beta subunit knockout (KO) mouse, which is a model of PPI-use, have lower bone mineral density (BMD) and impaired bone quality compared to wild type (WT) mice. Like PPI users, these KO mice display elevated gastric pH and hypergastrinemia, which in turn stimulates gastric histamine release. Previous studies have suggested a negative effect of histamine on bone, thus, we wanted to study whether a histamine 1 receptor (H1R) antagonist could improve bone quality in KO mice. Female KO and WT mice aged 8 weeks received either an H1R antagonist (cetirizine) or polyethylene glycol (PEG) for 6 months. At the end of the study, KO mice displayed elevated plasma histamine levels compared to WT. As demonstrated previously, the KO mice also exhibited lower whole body BMD, reduced mechanical bone strength, and impaired bone quality assessed by μCT. No significant differences, however, were found between the KO groups receiving cetirizine or PEG for any of the measured bone parameters. In vitro gene expression analyses of histamine receptors revealed the presence of H1R and H2R both in osteoblasts and osteoclasts, and H3R in late stage osteoblasts. In conclusion, administration of the H1R antagonist cetirizine in a concentration of 3 mg/kg did not rescue the osteoporotic phenotype in H(+) /K(+) ATPase beta subunit KO mice. It can, however, not be ruled out that histamine may influence bone via other receptors. J. Cell. Biochem. 117: 2089-2096, 2016. © 2016 Wiley Periodicals, Inc.

show abstract

Histamine stimulates production of osteoclast differentiation factor/receptor activator of nuclear factor-κB ligand by osteoblasts

Cited by 39 publications

References 38 publications

Histamine Promotes Osteoclastogenesis through the Differential Expression of Histamine Receptors on Osteoclasts and Osteoblasts

Histamine Promotes Osteoclastogenesis through the Differential Expression of Histamine Receptors on Osteoclasts and Osteoblasts

μ-Calpain Regulates Receptor Activator of NF-κB Ligand (RANKL)-supported Osteoclastogenesis via NF-κB Activation in RAW 264.7 Cells

Effects of the Histamine 1 Receptor Antagonist Cetirizine on the Osteoporotic Phenotype in H⁺/K⁺ATPase Beta Subunit KO Mice

Contact Info

Product

Resources

About

Histamine stimulates production of osteoclast differentiation factor/receptor activator of nuclear factor-κB ligand by osteoblasts

Cited by 39 publications

References 38 publications

Histamine Promotes Osteoclastogenesis through the Differential Expression of Histamine Receptors on Osteoclasts and Osteoblasts

Histamine Promotes Osteoclastogenesis through the Differential Expression of Histamine Receptors on Osteoclasts and Osteoblasts

μ-Calpain Regulates Receptor Activator of NF-κB Ligand (RANKL)-supported Osteoclastogenesis via NF-κB Activation in RAW 264.7 Cells

Effects of the Histamine 1 Receptor Antagonist Cetirizine on the Osteoporotic Phenotype in H+/K+ATPase Beta Subunit KO Mice

Contact Info

Product

Resources

About

Effects of the Histamine 1 Receptor Antagonist Cetirizine on the Osteoporotic Phenotype in H⁺/K⁺ATPase Beta Subunit KO Mice