Elcatonin prevents bone loss caused by skeletal unloading by inhibiting preosteoclast fusion through the unloading-induced high expression of calcitonin receptors in bone marrow cells

Bone ◽  
2016 ◽  
Vol 85 ◽  
pp. 70-80 ◽  
Author(s):  
Manabu Tsukamoto ◽  
Kunitaka Menuki ◽  
Teppei Murai ◽  
Akihisa Hatakeyama ◽  
Shinichiro Takada ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Loss ◽  
Bone Marrow Cells ◽  
High Expression ◽  
Skeletal Unloading ◽  
Calcitonin Receptors ◽  
Marrow Cells

scholarly journals Protocatechuic Acid Attenuates Trabecular Bone Loss in Ovariectomized Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Seon-A Jang ◽  
Hae Seong Song ◽  
Jeong Eun Kwon ◽  
Hyun Jin Baek ◽  
Hyun Jung Koo ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Loss ◽  
Trabecular Bone ◽  
Protocatechuic Acid ◽  
Bone Marrow Cells ◽  
Biomechanical Properties ◽  
Primary Osteoporosis ◽  
Nuclear Factor ◽  
Trabecular Bone Loss ◽  
Marrow Cells

Primary osteoporosis is a disease related to excessive bone resorption due to estrogen insufficiency that occurs postmenopause. Protocatechuic acid (PCA), or 3,4-dihydroxybenzoic acid, is a common compound present in numerous plants. Although numerous biological activities of PCA have been identified, its antiosteoporotic function has not been well established. In this study, the antiosteoporotic activity of PCA supplementation was determined in ovariectomized (OVX) female ICR mice at 12 weeks after OVX. The biomechanical properties of a bone were evaluated by microcomputed tomography. The signaling molecules associated with osteoclast differentiation were determined in bone marrow cells through immunoblot or RT-PCR. Oral supplementation with PCA (20 mg/kg/day) significantly ameliorated the OVX-mediated stimulation of osteoclast activity based on decreases in serum levels of receptor activator of nuclear factor κB ligand (RANKL), osteocalcin, and bone alkaline phosphatase and increase in serum osteoprotegerin (each group, n=6; p<0.05). In addition, the OVX-induced decreases in mRNA expression levels of cathepsin K, calcitonin receptor, nuclear factor of activated T cell cytoplasmic 1 (NFATc1), and tumor necrosis factor (TNF) receptor-associated factor-6 (TRAF6) in bone marrow cells were significantly attenuated (each group, n=6; p<0.05). Finally, the loss of trabecular bone and changes in biomechanical properties of a bone were significantly improved by supplementation with 20 mg/kg PCA (each group, n=6; p<0.05). Collectively, our results show that PCA supplement suppressed trabecular bone loss in OVX mice and therefore might be an effective alternative approach for preventing the progression of postmenopausal osteoporosis.

Climbing exercise enhances osteoblast differentiation and inhibits adipogenic differentiation with high expression of PTH/PTHrP receptor in bone marrow cells

Bone ◽  
2008 ◽  
Vol 43 (3) ◽  
pp. 613-620 ◽  
Author(s):  
Kunitaka Menuki ◽  
Toshiharu Mori ◽  
Akinori Sakai ◽  
Miyuki Sakuma ◽  
Nobukazu Okimoto ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Osteoblast Differentiation ◽  
Bone Marrow Cells ◽  
Adipogenic Differentiation ◽  
High Expression ◽  
Pthrp Receptor ◽  
Marrow Cells

scholarly journals Crif1 Promotes Osteoporosis in Mice after Radiation

2019 ◽  
Author(s):  
Lixin Xiang ◽  
Li Chen ◽  
Yang Xiang ◽  
Fengjie Li ◽  
Xiaomei Zhang ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Resorption ◽  
Bone Loss ◽  
Bone Marrow Cells ◽  
Current Knowledge ◽  
Osteoclast Differentiation ◽  
Protein Docking ◽  
Rankl Expression ◽  
Marrow Cells

AbstractRadiation induces rapid bone loss and enhances bone resorption and RANKL expression. RANKL provides the crucial signal to induce osteoclast differentiation and plays an important role in bone resorption. However, the mechanisms of radiation-induced osteoporosis are not fully understood. Here, we show that Crif1 expression increases in bone marrow cells after radiation. Conditional Crif1 deletion in bone marrow cells causes decreases in RANKL expression and the RANKL/OPG ratio, and relieves bone loss after radiation in mice. We further demonstrated in vitro that Crif1 promotes RANKL secretion via the cAMP/PKA pathway. Moreover, protein-protein docking screening identified five compounds as Crif1 inhibitors; these compounds dramatically suppressed RANKL secretion and CREB phosphorylation when cells were exposed to forskolin. This study enriches current knowledge of the pathogenesis of osteoporosis and provides insights into potential therapeutic strategies for osteoporosis treatment.

Continuous high expression of XBP1 and GRP78 is important for the survival of bone marrow cells in CCl4-treated cirrhotic liver

2008 ◽  
Vol 367 (3) ◽  
pp. 546-552 ◽  
Author(s):  
Yoshio Marumoto ◽  
Shuji Terai ◽  
Yohei Urata ◽  
Toshihiko Matsumoto ◽  
Yuko Mizunaga ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Cirrhotic Liver ◽  
High Expression ◽  
Marrow Cells

Induction of Calcitonin Receptors by lα, 25- Dihydroxyvitamin D3in Osteoclast-Like Multinucleated Cells Formed from Mouse Bone Marrow Cells*

Endocrinology ◽  
1988 ◽  
Vol 123 (3) ◽  
pp. 1504-1510 ◽  
Author(s):  
NAOYUKI TAKAHASHI ◽  
TAKUHIKO AKATSU ◽  
TAKAHISA SASAKI ◽  
GEOFF C. NICHOLSON ◽  
JANE M. MOSELEY ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Mouse Bone Marrow ◽  
Multinucleated Cells ◽  
Calcitonin Receptors ◽  
Mouse Bone Marrow Cells ◽  
Marrow Cells

scholarly journals Osteopontin is required for mechanical stress-dependent signals to bone marrow cells

2007 ◽  
Vol 193 (2) ◽  
pp. 235-243 ◽  
Author(s):  
Muneaki Ishijima ◽  
Kunikazu Tsuji ◽  
Susan R Rittling ◽  
Teruhito Yamashita ◽  
Hisashi Kurosawa ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Loss ◽  
Mechanical Stress ◽  
Bone Marrow Cells ◽  
Bone Matrix ◽  
Nodule Formation ◽  
Tail Suspension ◽  
Wild Type ◽  
Marrow Cells

Mechanical stress to bone plays a crucial role in the maintenance of bone homeostasis. It causes the deformation of bone matrix and generates strain force, which could initiate the mechano-transduction pathway. The presence of osteopontin (OPN), which is one of the abundant proteins in bone matrix, is required for the effects of mechanical stress on bone, as we have reported that OPN-null (OPN−/−) mice showed resistance to unloading-induced bone loss. However, cellular mechanisms underlying the phenomenon have not been completely elucidated. To obtain further insight into the role of OPN in mediating mechanical stress effect on bone, we examined in vitro mineralization and osteoclast-like cell formation in bone marrow cells obtained from hind limb bones of OPN−/− mice after tail suspension. The levels of mineralized nodule formation of bone marrow cells derived from the femora subjected to unloading were decreased compared with that from loaded control in wild-type mice. However, these were not decreased in cells from OPN−/− mice after tail suspension compared with that from loaded OPN−/− mice. Moreover, while spreading of osteoclast-like cells derived from bone marrow cells of the femora subjected to unloading was enhanced compared with that from loaded control in wild-type mice, this enhancement of spreading of these cells derived from the femora subjected to unloading was not recognized compared with those from loaded control in OPN−/− mice. These data provided cellular bases for the effect of the OPN deficiency on in vitro reduced mineralized nodule formation by osteoblasts and on enhancement of osteoclast spreading in vitro induced by the absence of mechanical stress. These in vitro results correlate well with the resistance to unloading-induced bone loss in OPN−/− mice in vivo, suggesting that OPN has an important role in the effects of unloading-induced alterations of differentiation of bone marrow into osteoblasts and osteoclasts.

CABG and intramyocardial delivery of CD133+ bone marrow cells: 3-years follow-up on safety and efficacy

2006 ◽  
Vol 54 (S 1) ◽  
Author(s):  
C Stamm ◽  
YH Choi ◽  
A Liebold ◽  
HD Kleine ◽  
S Dunkelmann ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Safety And Efficacy ◽  
Intramyocardial Delivery ◽  
Marrow Cells
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