Stimulation of osteoclastogenesis by enhanced levels of MIP-1α in BALB/c mice in vitro

Lee, Jieun; Shin, Hong Ju; Lee, Eun-A.; Phan, Tien Van; Choi, Hye-Seon

doi:10.1016/j.exphem.2007.04.006

Cited by 24 publications

(27 citation statements)

References 28 publications

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“…MIP-1 ␥ , which is upregulated in OC derived from RANKL-stimulated BMM, also promoted the survival of mature OC by activating NF-B ( 21 ). In our previous studies, neutralization of MIP-1 ␣ suppressed OC survival by M-CSF and RANKL, suggesting a critical role of MIP-1 ␣ in OC survival ( 35 ). Our present results also showed that M-CSF and RANKL induce OC survival in the absence of TLR4 and MyD88, suggesting that they did not share common signaling pathways with SFA, even with MIP-1 ␣ as a convergent molecule for OC survival.…”

Section: Discussionsupporting

confidence: 72%

“…Our previous data showing increased osteoclastogenesis in BALB/c mice, compared to that in C57BL/6 mice also suggested that MIP-1 ␣ is a potent osteoclastogenic factor for BMM. MIP-1 ␣ affected not only early precursors but also mature OC by preventing apoptosis ( 35 ), and a similar effect has been observed with other chemokines. SDF-1 prevented mature OC from undergoing apoptosis by altering the ratio of expression of Bcl-2 family members ( 36 ).…”

Section: Discussionmentioning

confidence: 50%

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Saturated fatty acids enhance osteoclast survival

Sul

Kim

et al. 2010

Journal of Lipid Research

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Section: Discussionsupporting

confidence: 72%

Section: Discussionmentioning

confidence: 50%

Saturated fatty acids enhance osteoclast survival

Sul

Kim

et al. 2010

Journal of Lipid Research

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“…Bone marrow cells were isolated from 4 to 5-weekold C57BL/6J mice as previously described. 16) All the mice were housed in the specific pathogen-free animal facility of the Immunomodulation Research Center, University of Ulsan. The animal experimentation protocols were approved by the Institutional Animal Care and Use Committee of the University of Ulsan Immunomodulation Research Center.…”

Section: Methodsmentioning

confidence: 99%

Gold Nanoparticles Inhibited the Receptor Activator of Nuclear Factor-κB Ligand (RANKL)-Induced Osteoclast Formation by Acting as an Antioxidant

Sul¹,

Kim²,

Kyung³

et al. 2010

Bioscience, Biotechnology, and Biochemistry

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105

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“…The bone ends were cut, and the marrow cavity was flushed out with ␣-MEM from one end of the bone, using a sterile 21-gauge needle. The bone marrow was further agitated using a Pasteur pipette to obtain a single-cell suspension, which was washed twice and incubated on plates with M-CSF (20 ng/ml, 416-ML; R&D Systems, Minneapolis, MN) for 16 h. Nonadherent cells were then harvested, layered on a Ficoll-Hypaque gradient, and cultured for two more days, by which time large populations of adherent monocyte/macrophagelike cells had formed on the bottom of the culture plates treated with M-CSF, as previously described (22). The few nonadherent cells were removed by washing the dishes with phosphate-buffered saline (PBS), and the adherent cells (bone marrow-derived macrophages, BMMs) were harvested using 0.02% EDTA and seeded at 8 ϫ 10 3 cells/well.…”

Section: Methodsmentioning

confidence: 99%

Overexpression of developmentally regulated GTP-binding protein-2 increases bone loss

Sul

Kim

et al. 2013

American Journal of Physiology-Endocrinology and Metabolism

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The developmentally regulated GTP-binding protein-2 (DRG2) is a novel subclass of GTPbinding proteins. Many functional characteristics of osteoclasts (OC) are associated with small GTPases. We hypothesized that DRG2 affects bone mass via modulating OC activity. Using DRG2 transgenic mice, we investigated the role of DRG2 in bone remodeling. DRG2 overexpression caused a decrease in bone mass and an increase in the number and activity of OC in vivo. DRG2 overexpression increased fusion, spreading, survival, and resorption activity of OC in vitro. Downregulation of DRG2 by siRNA decreased fusion, spreading, and survival of OC, supporting the observations found in DRG2 transgenic OC. Transgenic mature OCs were larger, with actin rings and higher ERK, Akt, Rac1 and Rho activities than wild-type OCs. Inhibition of these proteins abolished the effects of DRG2 on formation of large OCs with actin rings, implying that DRG2 affects cytoskeleton reorganization in a Rac1/Rho/ERK/Akt-dependent manner. In summary, DRG2 is associated with survival and cytoskeleton organization of OC under influence of macrophage colony-stimulating factor, and its overexpression leads to elevated bone resorptive activity of OC, resulting in bone loss. DRG2; osteoclast; fusion; spreading; bone resorption BONE UNDERGOES DYNAMIC REMODELING, and maintenance of bone mass and integrity requires a precise balance between bone resorption by osteoclasts (OC) and bone formation by osteoblasts. In osteoporosis, resorption exceeds formation, whereas osteopetrosis is due to defective OC formation and function. OC differentiation depends on at least two factors derived from stromal cells/osteoblasts: macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor-B ligand (RANKL) (3, 12). During differentiation, OCs become multinucleated by fusion, which plays a critical role in bone resorption (13). To actively resorb bone, OC forms an actin ring that is a complex molecular attachment structure that seals off an extracellular compartment located between the cell and resorbing bone (5). By virtue of tight sealing, the extracellular compartment is characterized by maintaining a low pH and enriching lysosomal enzymes that are required for digestion of the bone matrix.Many OC properties that are necessary for efficient bone resorption, such as actin ring formation, fusion, and cell survival, depend on the activity of small GTPases (6,15,16,36). The Rho family of GTPases plays a critical role in actin organization, with RhoA, Rac1, Cdc42, and RhoU being responsible for cytoskeletal organization and the polarization of OCs (6, 15, 36). The ARF GTPase family, known to regulate membrane trafficking and actin dynamics, is responsible for the regulation of the OC cytoskeleton and formation of the sealing zone (11). Decrease in Rac2 impairs migration and fusion required for OC and results in bone defects found in Shwachman-Diamond syndrome (24). The activity of Rac1 (9) and Ras (4) is essential for OC survival. Although several small GTPases have...

show abstract

Stimulation of osteoclastogenesis by enhanced levels of MIP-1α in BALB/c mice in vitro

Cited by 24 publications

References 28 publications

Saturated fatty acids enhance osteoclast survival

Saturated fatty acids enhance osteoclast survival

Gold Nanoparticles Inhibited the Receptor Activator of Nuclear Factor-κB Ligand (RANKL)-Induced Osteoclast Formation by Acting as an Antioxidant

Overexpression of developmentally regulated GTP-binding protein-2 increases bone loss

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