scholarly journals Methylation Status of a Single CpG Locus 3 Bases Upstream of TATA-Box of Receptor Activator of Nuclear Factor-κB Ligand (RANKL) Gene Promoter Modulates Cell- and Tissue-Specific RANKL Expression and Osteoclastogenesis

2007 ◽  
Vol 21 (1) ◽  
pp. 148-158 ◽  
Author(s):  
Riko Kitazawa ◽  
Sohei Kitazawa
Keyword(s):  
Methylation Status ◽  
Gene Promoter ◽  
Nuclear Factor Κb ◽  
Tata Box ◽  
Nuclear Factor ◽  
Rankl Expression ◽  
Tissue Specific ◽  
Receptor Activator

Rituximab abrogates joint destruction in rheumatoid arthritis by inhibiting osteoclastogenesis

2011 ◽  
Vol 71 (1) ◽  
pp. 108-113 ◽  
Author(s):  
Maria J H Boumans ◽  
Rogier M Thurlings ◽  
Lorraine Yeo ◽  
Dagmar Scheel-Toellner ◽  
Koen Vos ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Joint Destruction ◽  
Bone Destruction ◽  
Nuclear Factor Κb ◽  
Type I ◽  
Nuclear Factor ◽  
Rankl Expression ◽  
Osteoclast Precursors ◽  
Receptor Activator ◽  
Hands And Feet

ObjectivesTo examine how rituximab may result in the inhibition of joint destruction in rheumatoid arthritis (RA) patients.MethodsTwenty-eight patients with active RA were treated with rituximab. Radiographs of hands and feet before and 1 year after therapy were assessed using the Sharp–van der Heijde score (SHS). Expression of bone destruction markers was evaluated by immunohistochemistry and immunofluorescence of synovial biopsies obtained before and 16 weeks after the initiation of treatment. Serum levels of osteoprotegerin, receptor activator of nuclear factor κB ligand (RANKL), osteocalcin and cross-linked N-telopeptides of type I collagen (NTx) were measured by ELISA before and 16 weeks post-treatment.ResultsAfter 1 year, the mean (SD) change in total SHS was 1.4 (10.0). Sixteen weeks after treatment there was a decrease of 99% in receptor activator of nuclear factor κB-positive osteoclast precursors (p=0.02) and a decrease of 37% (p=0.016) in RANKL expression in the synovium and a trend towards reduced synovial osteoprotegerin expression (25%, p=0.07). In serum, both osteoprotegerin (20%, p=0.001) and RANKL (40%, p<0.0001) levels were significantly reduced 16 weeks after treatment, but the osteoprotegerin/RANKL ratio increased (157%, p=0.006). A trend was found towards an increase of osteocalcin levels (p=0.053), while NTx concentrations did not change.ConclusionsRituximab treatment is associated with a decrease in synovial osteoclast precursors and RANKL expression and an increase in the osteoprotegerin/RANKL ratio in serum. These observations may partly explain the protective effect of rituximab on the progression of joint destruction in RA.

scholarly journals Role of Prostaglandin E in Receptor Activator of Nuclear Factor-κB Ligand (RANKL) Expression in Osteoblasts Induced by Cell Adhesion to Bone Marrow B-lymphocytes

2009 ◽  
Vol 55 (5) ◽  
pp. 832-837 ◽  
Author(s):  
Michiko Hirata ◽  
Suguru Harada ◽  
Chiho Matsumoto ◽  
Morichika Takita ◽  
Chisato Miyaura ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cell Adhesion ◽  
B Lymphocytes ◽  
Nuclear Factor Κb ◽  
Prostaglandin E ◽  
Nuclear Factor ◽  
Rankl Expression ◽  
Receptor Activator

scholarly journals Colony-Stimulating Factor-1 (CSF-1) Directly Inhibits Receptor Activator of Nuclear Factor-κB Ligand (RANKL) Expression by Osteoblasts

Endocrinology ◽  
2009 ◽  
Vol 150 (11) ◽  
pp. 4977-4988 ◽  
Author(s):  
Y. Wittrant ◽  
Y. Gorin ◽  
S. Mohan ◽  
B. Wagner ◽  
S. L. Abboud-Werner
Keyword(s):  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Colony Stimulating Factor ◽  
Wild Type ◽  
Rankl Expression ◽  
Nadph Oxidase Activity ◽  
Rankl Mrna ◽  
Receptor Activator ◽  
Bone Marrow Cultures ◽  
Stimulating Factor

Colony-stimulating factor-1 (CSF-1), released by osteoblasts, stimulates the proliferation of osteoclast progenitors via the c-fms receptor (CSF-1R) and, in combination with receptor activator of nuclear factor-κB ligand (RANKL), leads to the formation of mature osteoclasts. Whether the CSF-1R is expressed by osteoblasts and mediates specific biological effects in osteoblasts has not been explored. Wild-type primary calvaria osteoblasts (OB) were analyzed for CSF-1R expression (RT-PCR and Western blot) and functionality (immunocomplex kinase assay). OB were serum starved for 24 h, and the effect of CSF-1 (0–100 ng/ml) on OB biological activities was determined at 48 h. In wild-type mouse bone marrow cultures, CSF-1 was tested for its effect on RANKL mRNA and osteoclast formation. Because ROS influence osteoblast RANKL expression, studies analyzed the effect of CSF-1 on reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and Nox1 and Nox4 proteins. Results indicate that OB express CSF-1R mRNA and protein and that CSF-1R could be phosphorylated in the presence of CSF-1. In osteoblasts, CSF-1 decreased RANKL mRNA in a dose- and time-dependent manner. Incubation of bone marrow cultures with CSF-1 resulted in a significant decline in tartrate-resistant acid phosphatase (TRACP) activity and CTR expression. RANKL-decreased expression by CSF-1 was correlated with a decrease of NADPH oxidase activity as well as Nox1 and Nox4 protein levels. These findings provide the first evidence that osteoblasts express CSF-1R and are a target for CSF-1 ligand. CSF-1-mediated inhibition of RANKL expression on osteoblasts may provide an important mechanism for coupling bone formation/resorption and preventing excessive osteoclastogenesis during normal skeletal growth.

Receptor Activator of Nuclear Factor-κB Ligand (RANKL) Expression in Hepatocellular Carcinoma With Bone Metastasis

2006 ◽  
Vol 14 (3) ◽  
pp. 1191-1199 ◽  
Author(s):  
Atsushi Sasaki ◽  
Kenji Ishikawa ◽  
Naotsugu Haraguchi ◽  
Hiroshi Inoue ◽  
Tetsuya Ishio ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Bone Metastasis ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Rankl Expression ◽  
Receptor Activator

scholarly journals Targeted Deletion of a Distant Transcriptional Enhancer of the Receptor Activator of Nuclear Factor-κB Ligand Gene Reduces Bone Remodeling and Increases Bone Mass

Endocrinology ◽  
2007 ◽  
Vol 149 (1) ◽  
pp. 146-153 ◽  
Author(s):  
Carlo Galli ◽  
Lee A. Zella ◽  
Jackie A. Fretz ◽  
Qiang Fu ◽  
J. Wesley Pike ◽  
...  
Keyword(s):  
Bone Mass ◽  
Bone Remodeling ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Rankl Expression ◽  
Transcriptional Enhancer ◽  
Dihydroxyvitamin D3 ◽  
Rankl Mrna ◽  
Receptor Activator ◽  
Stimulation Of

Receptor activator of nuclear factor-κB ligand (RANKL) is essential for osteoclast differentiation, and hormones and cytokines that stimulate bone resorption increase RANKL expression in stromal/osteoblastic cells. We have previously shown that PTH and 1,25-dihydroxyvitamin D3 control murine RANKL gene expression in vitro, in part, via an evolutionarily conserved transcriptional enhancer, designated the distal control region (DCR), located 76 kb upstream from the transcription start site. Herein we describe the phenotype of mice lacking this enhancer. Deletion of the DCR reduced PTH and 1,25-dihydroxyvitamin D3 stimulation of RANKL mRNA and osteoclast formation in primary bone marrow cultures as well as stimulation of RANKL mRNA in bone. DCR deletion also reduced basal RANKL mRNA levels in bone, thymus, and spleen. Moreover, mice lacking the DCR exhibited increased bone mass and strength. The increase in bone mass was due to reduced osteoclast and osteoblast formation leading to a low rate of bone remodeling similar to that observed in humans and mice with hypoparathyroidism. These findings demonstrate that hormonal control of RANKL expression via the DCR is a critical determinant of the rate of bone remodeling.

scholarly journals RANK and RANKL Expression in Salivary Gland Tumors

2020 ◽  
Vol 99 (7) ◽  
pp. 475-480
Author(s):  
Figen Aslan ◽  
Ülkü Küçük
Keyword(s):  
Salivary Gland ◽  
Malignant Tumors ◽  
Nuclear Factor Κb ◽  
Clinicopathological Features ◽  
Salivary Gland Tumors ◽  
Benign Tumors ◽  
Nuclear Factor ◽  
Rankl Expression ◽  
Positive Expression ◽  
Receptor Activator

Objectives: The pathogenesis and molecular basis of salivary gland tumors (SGT) are not well understood. We investigated the expression of receptor activator of nuclear factor κB (RANK) and RANK ligand (RANKL) in benign and malignant SGTs and their relationship with clinicopathological features. Methods: Fifty malignant and 38 benign SGTs were analyzed in this study. We evaluated the correlation between RANK and RANKL expression and benign and malignant tumors, as well as the correlation between clinicopathological prognostic parameters and RANK and RANKL expression. Results: Receptor activator of nuclear factor κB was positive in 82% (41) malignant SGTs and in 34.2% (13) benign SGTs. Receptor activator of nuclear factor κB ligand was expressed in 28% (14) malignant and 5.3% (2) benign tumors. Receptor activator of nuclear factor κB and RANKL expression were significantly different between benign and malignant SGTs ( P < .001, P = .006, respectively). However, a relationship was not found between positive expression of RANK or RANKL and clinicopathological features. Conclusions: In our study, RANK and RANKL expression was found to be higher in malignant SGTs compared to benign SGTs and RANK was more sensitive than RANKL. In addition, RANK and RANKL expression was higher in some malignant histological subtypes. Based on these results, we think that RANK and RANKL expression in SGTs and its potential as a target for treatment should continue to be investigated.

scholarly journals RANK (receptor activator of nuclear factor-κB) and RANKL expression in multiple myeloma

2002 ◽  
Vol 117 (1) ◽  
pp. 86-92 ◽  
Author(s):  
Sophie Roux ◽  
Véronique Meignin ◽  
Jeanine Quillard ◽  
Geri Meduri ◽  
Anne Guiochon-Mantel ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Rankl Expression ◽  
Receptor Activator
Sign in / Sign up

Export Citation Format

Share Document