scholarly journals RANKL (Receptor Activator of NFκB Ligand) Produced by Osteocytes Is Required for the Increase in B Cells and Bone Loss Caused by Estrogen Deficiency in Mice

2016 ◽  
Vol 291 (48) ◽  
pp. 24838-24850 ◽  
Author(s):  
Yuko Fujiwara ◽  
Marilina Piemontese ◽  
Yu Liu ◽  
Jeff D. Thostenson ◽  
Jinhu Xiong ◽  
...  
Keyword(s):  
B Cells ◽  
Bone Loss ◽  
Estrogen Deficiency ◽  
Receptor Activator

scholarly journals Ablation of p38α MAPK Signaling in Osteoblast Lineage Cells Protects Mice From Bone Loss Induced by Estrogen Deficiency

Endocrinology ◽  
2015 ◽  
Vol 156 (12) ◽  
pp. 4377-4387 ◽  
Author(s):  
Cyril Thouverey ◽  
Joseph Caverzasio
Keyword(s):  
Bone Loss ◽  
Nuclear Factor Κb ◽  
Mapk Signaling ◽  
Osteoclast Formation ◽  
Estrogen Deficiency ◽  
Nuclear Factor ◽  
Receptor Activator ◽  
P38α Mapk ◽  
Mapk Inhibitors ◽  
Osteoblast Lineage

Estrogen deficiency causes bone loss by increasing the number of bone-resorbing osteoclasts. Selective p38α MAPK inhibitors prevent bone-wasting effects of estrogen withdrawal but implicated mechanisms remain to be identified. Here, we show that inactivation of the p38α-encoding gene in osteoblast lineage cells with the use of an osteocalcin-cre transgene protects mice from ovariectomy-induced bone loss (a murine model of postmenopausal osteoporosis). Ovariectomy fails to induce bone loss, increase bone resorption, and stimulate receptor activator of nuclear factor κB ligand and IL-6 expression in mice lacking p38α in osteoblasts and osteocytes. Finally, TNFα or IL-1, which are osteoclastogenic cytokines overproduced in the bone marrow under estrogen deficiency, can activate p38α signaling in osteoblasts, but those cytokines cannot enhance Rankl and Il6 expressions or increase osteoclast formation in p38a-deficient osteoblast cultures. These findings demonstrate that p38α MAPK signaling in osteoblast lineage cells mediates ovariectomy-induced bone loss by up-regulating receptor activator of nuclear factor κB ligand and IL-6 production.

scholarly journals Mice lacking DKK1 in T cells exhibit high bone mass and are protected from estrogen deficiency-induced bone loss

iScience ◽  
2021 ◽  
pp. 102224
Author(s):  
Juliane Lehmann ◽  
Sylvia Thiele ◽  
Ulrike Baschant ◽  
Tilman D. Rachner ◽  
Christof Niehrs ◽  
...  
Keyword(s):  
T Cells ◽  
Bone Loss ◽  
Bone Mass ◽  
Estrogen Deficiency ◽  
High Bone Mass ◽  
High Bone

scholarly journals Nobiletin, a Polymethoxy Flavonoid, Suppresses Bone Resorption by Inhibiting NFκB-Dependent Prostaglandin E Synthesis in Osteoblasts and Prevents Bone Loss Due to Estrogen Deficiency

2011 ◽  
Vol 115 (1) ◽  
pp. 89-93 ◽  
Author(s):  
Suguru Harada ◽  
Tsukasa Tominari ◽  
Chiho Matsumoto ◽  
Michiko Hirata ◽  
Morichika Takita ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Estrogen Deficiency ◽  
Prostaglandin E

scholarly journals Porphyromonas gingivalis Infection-Associated Periodontal Bone Resorption Is Dependent on Receptor Activator of NF-κB Ligand

2013 ◽  
Vol 81 (5) ◽  
pp. 1502-1509 ◽  
Author(s):  
Xiaozhe Han ◽  
Xiaoping Lin ◽  
Xiaoqian Yu ◽  
Jiang Lin ◽  
Toshihisa Kawai ◽  
...  
Keyword(s):  
B Cells ◽  
Bone Resorption ◽  
Fusion Protein ◽  
Porphyromonas Gingivalis ◽  
Nuclear Factor Κb ◽  
Infected Group ◽  
T And B Cells ◽  
Content Type ◽  
Receptor Activator ◽  
Control Fusion

ABSTRACTPorphyromonas gingivalisis one of the oral microorganisms associated with human chronic periodontitis. The purpose of this study is to determine the role of the receptor activator of nuclear factor-κB ligand (RANKL) inP. gingivalisinfection-associated periodontal bone resorption. Inbred female Rowett rats were infected orally on four consecutive days (days 0 to 3) with 1 × 109P. gingivalisbacteria (strain ATCC 33277). Separate groups of rats also received an injection of anti-RANKL antibody, osteoprotegerin fusion protein (OPG-Fc), or a control fusion protein (L6-Fc) into gingival papillae in addition toP. gingivalisinfection. Robust serum IgG and salivary IgA antibody (P< 0.01) and T cell proliferation (P< 0.05) responses toP. gingivaliswere detected at day 7 and peaked at day 28 inP. gingivalis-infected rats. Both the concentration of soluble RANKL (sRANKL) in rat gingival tissues (P< 0.01) and periodontal bone resorption (P< 0.05) were significantly elevated at day 28 in theP. gingivalis-infected group compared to levels in the uninfected group. Correspondingly, RANKL-expressing T and B cells in rat gingival tissues were significantly increased at day 28 in theP. gingivalis-infected group compared to the levels in the uninfected group (P< 0.01). Injection of anti-RANKL antibody (P< 0.05) or OPG-Fc (P< 0.01), but not L6-Fc, into rat gingival papillae afterP. gingivalisinfection resulted in significantly reduced periodontal bone resorption. This study suggests thatP. gingivalisinfection-associated periodontal bone resorption is RANKL dependent and is accompanied by increased local infiltration of RANKL-expressing T and B cells.

scholarly journals An IL-7-dependent rebound in thymic T cell output contributes to the bone loss induced by estrogen deficiency

2005 ◽  
Vol 102 (46) ◽  
pp. 16735-16740 ◽  
Author(s):  
M. R. Ryan ◽  
R. Shepherd ◽  
J. K. Leavey ◽  
Y. Gao ◽  
F. Grassi ◽  
...  
Keyword(s):  
T Cell ◽  
Bone Loss ◽  
Estrogen Deficiency

scholarly journals Metabolomic Profiles Delineate Signature Metabolic Shifts during Estrogen Deficiency-Induced Bone Loss in Rat by GC-TOF/MS

PLoS ONE ◽  
2013 ◽  
Vol 8 (2) ◽  
pp. e54965 ◽  
Author(s):  
Bo Ma ◽  
Jiannan Liu ◽  
Qi Zhang ◽  
Hanjie Ying ◽  
Jiye A ◽  
...  
Keyword(s):  
Bone Loss ◽  
Estrogen Deficiency ◽  
Tof Ms
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