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Journal articles on the topic 'Osteoclasts'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Combs, Charlotte E., Karen Fuller, Hashethra Kumar, et al. "Urocortin is a novel regulator of osteoclast differentiation and function through inhibition of a canonical transient receptor potential 1-like cation channel." Journal of Endocrinology 212, no. 2 (2011): 187–97. http://dx.doi.org/10.1530/joe-11-0254.

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This study investigated the role of urocortin (UCN), a member of the corticotrophin-releasing factor (CRF) family of peptides, in osteoclast maturation and function. We found that 10−7 M UCN significantly (P<0.05) suppressed osteoclast differentiation from bone marrow precursor cells in culture and reduced the expression of several osteoclastic markers. Furthermore, UCN potently suppressed osteoclast bone resorption, by significantly inhibiting both the plan area of bone resorbed by osteoclasts and actin ring formation within osteoclasts at 10−9 M (P<0.05), with complete inhibition at 10

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2

Alatalo, Sari L., Jussi M. Halleen, Teuvo A. Hentunen, Jukka Mönkkönen, and H. Kalervo Väänänen. "Rapid Screening Method for Osteoclast Differentiation in Vitro That Measures Tartrate-resistant Acid Phosphatase 5b Activity Secreted into the Culture Medium." Clinical Chemistry 46, no. 11 (2000): 1751–54. http://dx.doi.org/10.1093/clinchem/46.11.1751.

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Abstract Background: Osteoclasts secrete tartrate-resistant acid phosphatase (TRAP; EC 3.1.3.2) 5b into the circulation. We studied the release of TRAP 5b from osteoclasts using a mouse in vitro osteoclast differentiation assay. Methods: We developed and characterized a polyclonal antiserum in rabbits, using purified human osteoclastic TRAP 5b as antigen. The antiserum was specific for TRAP in Western analysis of mouse osteoclast culture medium and was used to develop an immunoassay. We cultured mouse bone marrow-derived osteoclast precursor cells for 3–7 days with or without clodronate in the

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3

Niida, Shumpei, Masato Kaku, Hitoshi Amano, et al. "Vascular Endothelial Growth Factor Can Substitute for Macrophage Colony-Stimulating Factor in the Support of Osteoclastic Bone Resorption." Journal of Experimental Medicine 190, no. 2 (1999): 293–98. http://dx.doi.org/10.1084/jem.190.2.293.

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We demonstrated previously that a single injection of recombinant human macrophage colony-stimulating factor (rhM-CSF) is sufficient for osteoclast recruitment and survival in osteopetrotic (op/op) mice with a deficiency in osteoclasts resulting from a mutation in M-CSF gene. In this study, we show that a single injection of recombinant human vascular endothelial growth factor (rhVEGF) can similarly induce osteoclast recruitment in op/op mice. Osteoclasts predominantly expressed VEGF receptor 1 (VEGFR-1), and activity of recombinant human placenta growth factor 1 on osteoclast recruitment was

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4

Fuller, K., and T. J. Chambers. "Localisation of mRNA for collagenase in osteocytic, bone surface and chondrocytic cells but not osteoclasts." Journal of Cell Science 108, no. 6 (1995): 2221–30. http://dx.doi.org/10.1242/jcs.108.6.2221.

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Osteoclasts resorb the extracellular matrix of bone by secreting protons and enzymes into a circumpherentially sealed compartment between the osteoclast and the bone surface. Although the lysosomal cysteine proteinases play a major role in matrix degradation by osteoclasts, collagenase (matrix metalloproteinase-1, EC 3.4.24.7) is also required for osteoclastic bone resorption, and may be directly involved in collagen degradation in the hemivacuole. We assessed the effects of inhibitors of cysteine proteinases and collagenase on bone resorption by osteoclasts isolated from rodent bone. We found

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Fuller, Karen, Brian Wong, Simon Fox, Yongwon Choi, and Tim J. Chambers. "TRANCE Is Necessary and Sufficient for Osteoblast-mediated Activation of Bone Resorption in Osteoclasts." Journal of Experimental Medicine 188, no. 5 (1998): 997–1001. http://dx.doi.org/10.1084/jem.188.5.997.

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TRANCE (tumor necrosis factor–related activation-induced cytokine) is a recently described member of the tumor necrosis factor superfamily that stimulates dendritic cell survival and has also been found to induce osteoclastic differentiation from hemopoietic precursors. However, its effects on mature osteoclasts have not been defined. It has long been recognized that stimulation of osteoclasts by agents such as parathyroid hormone (PTH) occurs through a hormonal interaction with osteoblastic cells, which are thereby induced to activate osteoclasts. To determine whether TRANCE accounts for this

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Fuller, Karen, Chiho Murphy, Barrie Kirstein, Simon W. Fox та Timothy J. Chambers. "TNFα Potently Activates Osteoclasts, through a Direct Action Independent of and Strongly Synergistic with RANKL". Endocrinology 143, № 3 (2002): 1108–18. http://dx.doi.org/10.1210/endo.143.3.8701.

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Abstract TNFα is pivotal to the pathogenesis of inflammatory and possibly postmenopausal osteolysis. Much recent work has clarified mechanisms by which TNFα promotes osteoclastogenesis, but the means by which it activates osteoclasts to resorb bone remain uncertain. We found that very low concentrations of TNFα promoted actin ring formation, which correlates with functional activation in osteoclasts, both in osteoclasts formed in vitro and extracted from newborn rats. TNFα was equipotent with RANKL for this action. Activation by TNFα was unaffected by blockade of RANKL by OPG, its soluble deco

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7

Yu, Anna Xiao-Dan, Jian Xiao, Shi-Zheng Zhao, et al. "Biological Evaluation and Transcriptomic Analysis of Corylin as an Inhibitor of Osteoclast Differentiation." International Journal of Molecular Sciences 22, no. 7 (2021): 3540. http://dx.doi.org/10.3390/ijms22073540.

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Corylin, a flavonoid isolated from the fruit of Psoralea corylifolia, has an osteogenic effect on osteoblasts in vitro and bone micromass ex vivo. However, the effect and mechanism of corylin in regulating osteoclastogenesis remain unknown. By using murine bone marrow macrophages as the osteoclast precursor, corylin was found to inhibit the receptor activator of nuclear factor (NF) κB ligand (RANKL)-induced osteoclast differentiation via down-regulating osteoclastic marker genes. In parallel, F-actin formation and osteoclast migration were diminished in corylin-treated cultured osteoclasts, an

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8

Nakamura, I., M. F. Pilkington, P. T. Lakkakorpi, et al. "Role of alpha(v)beta(3) integrin in osteoclast migration and formation of the sealing zone." Journal of Cell Science 112, no. 22 (1999): 3985–93. http://dx.doi.org/10.1242/jcs.112.22.3985.

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The alpha(v)beta(3) integrin is abundantly expressed in osteoclasts and has been implicated in the regulation of osteoclast function, especially in cell attachment. However, in vivo studies have shown that echistatin, an RGD-containing disintegrin which binds to alpha(v)beta(3), inhibits bone resorption without changing the number of osteoclasts on the bone surface, suggesting inhibition of osteoclast activity. The objective of this study was to examine how occupancy of alpha(v)beta(3) integrins inhibits osteoclast function, using primary rat osteoclasts and murine pre-fusion osteoclast-like c

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9

Kameda, Takashi, Hiroshi Mano, Tatsuhisa Yuasa, et al. "Estrogen Inhibits Bone Resorption by Directly Inducing Apoptosis of the Bone-resorbing Osteoclasts." Journal of Experimental Medicine 186, no. 4 (1997): 489–95. http://dx.doi.org/10.1084/jem.186.4.489.

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Estrogen deficiency causes bone loss, which can be prevented by estrogen replacement therapy. Using a recently developed technique for isolation of highly purified mammalian osteoclasts, we showed that 17 β-estradiol (E2) was able to directly inhibit osteoclastic bone resorption. At concentrations effective for inhibiting bone resorption, E2 also directly induced osteoclast apoptosis in a dose- and time-dependent manner. ICI164,384 and tamoxifen, as pure and partial antagonists, respectively, completely or partially blocked the effect of E2 on both inhibition of osteoclastic bone resorption an

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10

Fuller, K., J. M. Owens, and T. J. Chambers. "Macrophage inflammatory protein-1 alpha and IL-8 stimulate the motility but suppress the resorption of isolated rat osteoclasts." Journal of Immunology 154, no. 11 (1995): 6065–72. http://dx.doi.org/10.4049/jimmunol.154.11.6065.

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Abstract Cells of the osteoblastic lineage play a major role in the regulation of osteoclastic bone resorption. Recent studies have demonstrated production of chemokines by osteoblastic cells. Although these phagocyte-stimulating and proinflammatory cytokines act as chemoattractants and activators for other members of the hemopoietic lineage, their actions on osteoclasts have not been characterized. We found that macrophage inflammatory protein-1 alpha (MIP-1 alpha) and IL-8 inhibited bone resorption by rat osteoclasts, primarily through reduction in the proportion of osteoclasts resorbing bon

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11

Perkins, S. L., and S. J. Kling. "Local concentrations of macrophage colony-stimulating factor mediate osteoclastic differentiation." American Journal of Physiology-Endocrinology and Metabolism 269, no. 6 (1995): E1024—E1030. http://dx.doi.org/10.1152/ajpendo.1995.269.6.e1024.

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Macrophage colony-stimulating factor (M-CSF) is essential for differentiation of osteoclasts and macrophages from a common bone marrow precursor. Using ST-2 stromal cell/murine bone marrow coculture, we studied the effects of increasing amounts of M-CSF on differentiation of macrophages and osteoclasts. Addition of exogenous M-CSF caused a dose-dependent 98% decrease in tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells, accompanied by a 2.5-fold increase in nonspecific esterase-staining macrophages. Similar decrease in osteoclastic functional activity, including 125I-lab

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12

Lerner, Ulf H. "New Molecules in the Tumor Necrosis Factor Ligand and Receptor Superfamilies with Importance for Physiological and Pathological Bone Resorption." Critical Reviews in Oral Biology & Medicine 15, no. 2 (2004): 64–81. http://dx.doi.org/10.1177/154411130401500202.

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Osteoclasts are tissue-specific polykaryon bone-resorbing cells derived from the monocyte/macrophage hematopoietic lineage with specialized functions required for the adhesion of the cells to bone and the subsequent polarization of the cell membrane, secretion of acid to dissolve mineral crystals, and release of proteolytic enzymes to degrade the extracellular matrix proteins. Most pathological conditions in the skeleton lead to loss of bone due to excess osteoclastic bone resorption, including periodontal disease, rheumatoid arthritis, and osteoporosis. In rare cases, most of them genetic, pa

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13

Fuller, K., J. M. Owens, C. J. Jagger, A. Wilson, R. Moss, and T. J. Chambers. "Macrophage colony-stimulating factor stimulates survival and chemotactic behavior in isolated osteoclasts." Journal of Experimental Medicine 178, no. 5 (1993): 1733–44. http://dx.doi.org/10.1084/jem.178.5.1733.

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Macrophage colony-stimulating factor (M-CSF) is known to play an important role in osteoclast formation. However, its actions on mature cells have not been fully characterized. We now report that M-CSF dramatically stimulates osteoclastic motility and spreading; osteoclasts responded to a gradient of M-CSF with orientation, and random cell polarization occurred after isotropic exposure. M-CSF also supported the survival of osteoclasts by preventing apoptosis. Paradoxically, M-CSF inhibits bone resorption by isolated osteoclasts. We found that this was effected predominantly by reduction in the

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14

Andersson, G. N., and S. C. Marks. "Tartrate-resistant acid ATPase as a cytochemical marker for osteoclasts." Journal of Histochemistry & Cytochemistry 37, no. 1 (1989): 115–17. http://dx.doi.org/10.1177/37.1.2461980.

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We present a modified histochemical method for staining osteoclasts and adjacent mononuclear cells which takes advantage of the recently described substrate specificity for ATP of osteoclastic acid phosphatase. Staining of osteoclasts using ATP as substrate exhibits by light microscopy the same tartrate resistance as conventional acidic phosphatases, without the bone surface staining seen with other substrates. This feature, coupled with specific staining of fewer vicinal mononuclear cells, makes this method potentially useful for studying osteoclast ontogeny and function.

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15

Heinemann, Christiane, Josephine Adam, Benjamin Kruppke, Vera Hintze, Hans-Peter Wiesmann, and Thomas Hanke. "How to Get Them off?—Assessment of Innovative Techniques for Generation and Detachment of Mature Osteoclasts for Biomaterial Resorption Studies." International Journal of Molecular Sciences 22, no. 3 (2021): 1329. http://dx.doi.org/10.3390/ijms22031329.

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The fusion process of mononuclear monocytes into multinuclear osteoclasts in vitro is an essential process for the study of osteoclastic resorption of biomaterials. Thereby biomaterials offer many influencing factors such as sample shape, material composition, and surface topography, which can have a decisive influence on the fusion and thus the entire investigation. For the specific investigation of resorption, it can therefore be advantageous to skip the fusion on samples and use mature, predifferentiated osteoclasts directly. However, most conventional detachment methods (cell scraper, accu

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16

Møller, Anaïs M. J., Jean-Marie Delaissé, Jacob B. Olesen, et al. "Fusion Potential of Human Osteoclasts In Vitro Reflects Age, Menopause, and In Vivo Bone Resorption Levels of Their Donors—A Possible Involvement of DC-STAMP." International Journal of Molecular Sciences 21, no. 17 (2020): 6368. http://dx.doi.org/10.3390/ijms21176368.

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It is well established that multinucleation is central for osteoclastic bone resorption. However, our knowledge on the mechanisms regulating how many nuclei an osteoclast will have is limited. The objective of this study was to investigate donor-related variations in the fusion potential of in vitro-generated osteoclasts. Therefore, CD14+ monocytes were isolated from 49 healthy female donors. Donor demographics were compared to the in vivo bone biomarker levels and their monocytes’ ability to differentiate into osteoclasts, showing that: (1) C-terminal telopeptide of type I collagen (CTX) and

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17

Moreaux, Jerome, Dirk Hose, Alboukadel Kassambara, et al. "Osteoclast-gene expression profiling reveals osteoclast-derived CCR2 chemokines promoting myeloma cell migration." Blood 117, no. 4 (2011): 1280–90. http://dx.doi.org/10.1182/blood-2010-04-279760.

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Abstract Multiple myeloma is characterized by the clonal expansion of malignant plasma cells (multiple myeloma cells [MMCs]), in the bone marrow. Osteolytic bone lesions are detected in 80% of patients because of increased osteoclastic bone resorption and reduced osteoblastic bone formation. MMCs are found closely associated with sites of increased bone resorption. Osteoclasts strongly support MMC survival in vitro. To further elucidate the mechanisms involved in osteoclast/MMC interaction, we have identified 552 genes overexpressed in osteoclasts compared with other bone marrow cell subpopula

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Miyauchi, Yoshiteru, Ken Ninomiya, Hiroya Miyamoto, et al. "The Blimp1–Bcl6 axis is critical to regulate osteoclast differentiation and bone homeostasis." Journal of Experimental Medicine 207, no. 4 (2010): 751–62. http://dx.doi.org/10.1084/jem.20091957.

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Controlling osteoclastogenesis is critical to maintain physiological bone homeostasis and prevent skeletal disorders. Although signaling activating nuclear factor of activated T cells 1 (NFATc1), a transcription factor essential for osteoclastogenesis, has been intensively investigated, factors antagonistic to NFATc1 in osteoclasts have not been characterized. Here, we describe a novel pathway that maintains bone homeostasis via two transcriptional repressors, B cell lymphoma 6 (Bcl6) and B lymphocyte–induced maturation protein-1 (Blimp1). We show that Bcl6 directly targets ‘osteoclastic’ mole

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19

Cheng, Yin, Haixia Liu, Jing Li, et al. "Evaluation of culture conditions for osteoclastogenesis in RAW264.7 cells." PLOS ONE 17, no. 11 (2022): e0277871. http://dx.doi.org/10.1371/journal.pone.0277871.

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Osteoclasts are the only multinucleated cells in vivo responsible for bone resorption and are vital for regulating bone remodeling and maintaining bone mass. The RAW264.7 cell line is widely used to study osteoclastic differentiation and biological molecular mechanism. However, protocols for inducing osteoclast formation in RAW264.7 cells vary considerably between laboratories, hindering the replication of results. Therefore, we tested the influence of culture conditions on osteoclast differentiation, including cell density and receptor activator of nuclear factor kappa-B ligand (RANKL) concen

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Huang, WH, AT Lau, LL Daniels, et al. "Detection of estrogen receptor alpha, carbonic anhydrase II and tartrate-resistant acid phosphatase mRNAs in putative mononuclear osteoclast precursor cells of neonatal rats by fluorescence in situ hybridization." Journal of Molecular Endocrinology 20, no. 2 (1998): 211–19. http://dx.doi.org/10.1677/jme.0.0200211.

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Increasing evidence suggests that estrogen deficiency in women promotes the expansion of populations of bone marrow cells that differentiate into osteoclasts under the influence of osteotropic hormones and local factors. A progressive cytoplasmic accumulation of osteoclastic bone resorbing enzymes, such as tartrate-resistant acid phosphatase (TRACP) and carbonic anhydrase II (CA II), characterizes osteoclast differentiation. To evaluate the possibility that estrogen may have a direct effect on osteoclast precursor cells, we investigated the mRNA levels of estrogen receptor a (ERa), TRACP and C

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Hulley, Philippa A., and Helen J. Knowles. "A New Method to Sort Differentiating Osteoclasts into Defined Homogeneous Subgroups." Cells 11, no. 24 (2022): 3973. http://dx.doi.org/10.3390/cells11243973.

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Osteoclasts regulate skeletal development but also drive pathological osteolysis, making them prime therapeutic targets. Osteoclast research is limited by the heterogeneity of osteoclast populations generated in vitro, where the mixture of undifferentiated monocytes, binuclear pre-osteoclasts and multinucleated osteoclasts has by necessity been considered a single osteoclast population. This study describes the differentiation of primary human CD14+ monocyte-derived osteoclasts in 3D collagen gels. These osteoclasts remained small (>95% with ≤5 nuclei) but were viable and active; when relea

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22

Martin-Millan, Marta, Maria Almeida, Elena Ambrogini та ін. "The Estrogen Receptor-α in Osteoclasts Mediates the Protective Effects of Estrogens on Cancellous But Not Cortical Bone". Molecular Endocrinology 24, № 2 (2010): 323–34. http://dx.doi.org/10.1210/me.2009-0354.

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Abstract Estrogens attenuate osteoclastogenesis and stimulate osteoclast apoptosis, but the molecular mechanism and contribution of these effects to the overall antiosteoporotic efficacy of estrogens remain controversial. We selectively deleted the estrogen receptor (ER)α from the monocyte/macrophage cell lineage in mice (ERαLysM−/−) and found a 2-fold increase in osteoclast progenitors in the marrow and the number of osteoclasts in cancellous bone, along with a decrease in cancellous bone mass. After loss of estrogens these mice failed to exhibit the expected increase in osteoclast progenitor

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Dai, Jingjin, Rui Dong, Xinyun Han, et al. "Osteoclast-derived exosomal let-7a-5p targets Smad2 to promote the hypertrophic differentiation of chondrocytes." American Journal of Physiology-Cell Physiology 319, no. 1 (2020): C21—C33. http://dx.doi.org/10.1152/ajpcell.00039.2020.

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The invasion of osteoclasts into the cartilage via blood vessels advances the process of endochondral ossification, and dysregulation of dynamic intercellular interactions results in skeletal dysplasias. Although the regulation of osteoclasts by growth plate chondrocytes has been reported in detail, the effect of osteoclasts on chondrocytes remains to be determined. In this study, ATDC5 cells and bone marrow mesenchymal stem cells were differentiated into chondrocytes and treated with conditioned medium obtained from bone marrow macrophages differentiated to osteoclast precursors and osteoclas

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Lee, Kyunghee, Incheol Seo, Mun Choi, and Daewon Jeong. "Roles of Mitogen-Activated Protein Kinases in Osteoclast Biology." International Journal of Molecular Sciences 19, no. 10 (2018): 3004. http://dx.doi.org/10.3390/ijms19103004.

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Bone undergoes continuous remodeling, which is homeostatically regulated by concerted communication between bone-forming osteoblasts and bone-degrading osteoclasts. Multinucleated giant osteoclasts are the only specialized cells that degrade or resorb the organic and inorganic bone components. They secrete proteases (e.g., cathepsin K) that degrade the organic collagenous matrix and establish localized acidosis at the bone-resorbing site through proton-pumping to facilitate the dissolution of inorganic mineral. Osteoporosis, the most common bone disease, is caused by excessive bone resorption,

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Huang, W. H., L. L. Daniels, D. J. Wood, U. Seydel, J. M. Papadimitriou, and M. H. Zheng. "VITAMIN D RECEPTOR mRNA IS EXPRESSED IN OSTEOCLAST-LIKE CELLS OF HUMAN GIANT CELL TUMOR OF BONE (OSTEOCLASTOMA)." Journal of Musculoskeletal Research 03, no. 03 (1999): 201–7. http://dx.doi.org/10.1142/s021895779900021x.

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The conventional view of the effects of 1,25- (OH)2D3 on osteoclastogenesis and bone resorption are thought to be mediated by stromal cells or osteoblastic cell. Giant cell tumor of bone (GCT) is characterized by multinuclear giant cells (osteoclast-like cells) distributed among a mass of mononuclear cells. Because it is very difficult to obtain normal human osteoclasts, many investigators, including ourselves, have used GCT as a source of human osteoclasts to enhance the understanding of normal skeletal remodeling and especially the hormone regulation of osteoclast functions. In this report,

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Yagi, Mitsuru, Takeshi Miyamoto, Yumi Sawatani, et al. "DC-STAMP is essential for cell–cell fusion in osteoclasts and foreign body giant cells." Journal of Experimental Medicine 202, no. 3 (2005): 345–51. http://dx.doi.org/10.1084/jem.20050645.

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Osteoclasts are bone-resorbing cells that play a pivotal role in bone remodeling. Osteoclasts form large multinuclear giant cells by fusion of mononuclear osteoclasts. How cell fusion is mediated, however, is unclear. We identify the dendritic cell–specific transmembrane protein (DC-STAMP), a putative seven-transmembrane protein, by a DNA subtraction screen between multinuclear osteoclasts and mononuclear macrophages. DC-STAMP is highly expressed in osteoclasts but not in macrophages. DC-STAMP–deficient mice were generated, and osteoclast cell fusion was completely abrogated in homozygotes des

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Gwaltney, S. M., R. J. S. Galvin, K. B. Register, R. B. Rimler, and M. R. Ackermann. "Effects of Pasteurella multocida Toxin on Porcine Bone Marrow Cell Differentiation into Osteoclasts and Osteoblasts." Veterinary Pathology 34, no. 5 (1997): 421–30. http://dx.doi.org/10.1177/030098589703400506.

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The effect of Pasteurella multocida toxin (PMT) on porcine osteoclast and osteoblast differentiation was studied using in vitro cell culture systems. When grown in the presence of Vitamin D3, isolated porcine bone marrow cells formed multinucleated cells with features characteristic of osteoclasts. Exposure of bone marrow cells to Vitamin D3 and PMT during growth resulted in formation of increased numbers and earlier appearance of osteoclasts compared to controls. Ultrafiltered medium from PMT-treated cells likewise increased osteoclast numbers, suggesting that a soluble mediator may be involv

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Hatton, R., M. Stimpel, and T. J. Chambers. "Angiotensin II is generated from angiotensin I by bone cells and stimulates osteoclastic bone resorption in vitro." Journal of Endocrinology 152, no. 1 (1997): 5–10. http://dx.doi.org/10.1677/joe.0.1520005.

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Abstract During bone resorption, osteoclasts are closely associated with endothelial cells. The latter are able to produce several agents that regulate bone resorption. In view of the increasing evidence that angiotensin II, which can be generated by endothelial cells, has actions outside the traditional renin-angiotensin system, we tested the effect of angiotensin II on bone resorption. Angiotensin II showed no effect either on osteoclast formation or on bone resorption by isolated osteoclasts. However, in co-cultures of osteoclasts with calvarial or MC3T3-E1 osteoblastic cells, and in osteoc

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Na, Woojin, Eun-Jung Lee, Min-Kyung Kang, et al. "Aesculetin Inhibits Osteoclastic Bone Resorption through Blocking Ruffled Border Formation and Lysosomal Trafficking." International Journal of Molecular Sciences 21, no. 22 (2020): 8581. http://dx.doi.org/10.3390/ijms21228581.

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For the optimal resorption of mineralized bone matrix, osteoclasts require the generation of the ruffled border and acidic resorption lacuna through lysosomal trafficking and exocytosis. Coumarin-type aesculetin is a naturally occurring compound with anti-inflammatory and antibacterial effects. However, the direct effects of aesculetin on osteoclastogenesis remain to be elucidated. This study found that aesculetin inhibited osteoclast activation and bone resorption through blocking formation and exocytosis of lysosomes. Raw 264.7 cells were differentiated in the presence of 50 ng/mL receptor a

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Feng, Shengmei, Lianfu Deng, Wei Chen, Jianzhong Shao, Guoliang Xu, and Yi-Ping Li. "Atp6v1c1 is an essential component of the osteoclast proton pump and in F-actin ring formation in osteoclasts." Biochemical Journal 417, no. 1 (2008): 195–203. http://dx.doi.org/10.1042/bj20081073.

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Bone resorption relies on the extracellular acidification function of V-ATPase (vacuolar-type proton-translocating ATPase) proton pump(s) present in the plasma membrane of osteoclasts. The exact configuration of the osteoclast-specific ruffled border V-ATPases remains largely unknown. In the present study, we found that the V-ATPase subunit Atp6v1c1 (C1) is highly expressed in osteoclasts, whereas subunits Atp6v1c2a (C2a) and Atp6v1c2b (C2b) are not. The expression level of C1 is highly induced by RANKL [receptor activator for NF-κB (nuclear factor κB) ligand] during osteoclast differentiation

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Roy, Michèle, and Sophie Roux. "Rab GTPases in Osteoclastic Bone Resorption and Autophagy." International Journal of Molecular Sciences 21, no. 20 (2020): 7655. http://dx.doi.org/10.3390/ijms21207655.

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Small guanosine triphosphate hydrolases (GTPases) of the Rab family are involved in plasma membrane delivery, fusion events, and lysosomal and autophagic degradation pathways, thereby regulating signaling pathways and cell differentiation and function. Osteoclasts are bone-resorbing cells that maintain bone homeostasis. Polarized vesicular trafficking pathways result in the formation of the ruffled border, the osteoclast’s resorptive organelle, which also assists in transcytosis. Here, we reviewed the different roles of Rab GTPases in the endomembrane machinery of osteoclasts and in bone disea

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Ewanchuk, Benjamin W., Corey R. Arnold, Dale R. Balce та ін. "A non-immunological role for γ-interferon–inducible lysosomal thiol reductase (GILT) in osteoclastic bone resorption". Science Advances 7, № 17 (2021): eabd3684. http://dx.doi.org/10.1126/sciadv.abd3684.

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The extracellular bone resorbing lacuna of the osteoclast shares many characteristics with the degradative lysosome of antigen-presenting cells. γ-Interferon–inducible lysosomal thiol reductase (GILT) enhances antigen processing within lysosomes through direct reduction of antigen disulfides and maintenance of cysteine protease activity. In this study, we found the osteoclastogenic cytokine RANKL drove expression of GILT in osteoclast precursors in a STAT1-dependent manner, resulting in high levels of GILT in mature osteoclasts, which could be further augmented by γ-interferon. GILT colocalize

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Kim, Tae-Ho, Chae Gyeong Jeong, Hyeong-U. Son, et al. "Ethanolic Extract of Rubus coreanus Fruits Inhibits Bone Marrow-Derived Osteoclast Differentiation and Lipopolysaccharide-Induced Bone Loss." Natural Product Communications 12, no. 12 (2017): 1934578X1701201. http://dx.doi.org/10.1177/1934578x1701201228.

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The inhibition of osteoclast differentiation/bone resorption is a well-known therapeutic strategy for controlling pathological and postmenopausal bone loss. Natural products that specifically inhibit osteoclastogenesis could therefore be developed as antiresorptive drugs for the treatment of metabolic bone disorders characterized by excessive osteoclastic bone resorption. We therefore examined the effects of Rubus coreanus extract (eeRc) on receptor activator of nuclear factor kappa-B ligand (RANKL)-induced differentiation of bone marrow macrophages (BMMs) into osteoclasts and pit formation in

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Athanasou, N. A., J. Quinn, A. Heryet, and J. O. McGee. "Localization of platelet antigens and fibrinogen on osteoclasts." Journal of Cell Science 89, no. 1 (1988): 115–22. http://dx.doi.org/10.1242/jcs.89.1.115.

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The antigenic phenotype of the human osteoclast, which is known to be derived from a circulating mononuclear precursor cell of haemopoietic origin, is controversial. Recent studies have shown that macrophage as well as megakaryocyte/platelet antigens are expressed by osteoclasts. In this study, we have sought to define, by immunohistochemistry, the nature and possible function of platelet antigens expressed by human osteoclasts in foetal and adult bone specimens. Monoclonal antibodies to platelet glycoprotein IIIa (gpIIIa) and CD9 antibodies stained osteoclasts in all bone specimens examined.

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Hayashi, Shin-Ichi, Toshiyuki Yamane, Akitomo Miyamoto, et al. "Commitment and differentiation of stem cells to the osteoclast lineage." Biochemistry and Cell Biology 76, no. 6 (1998): 911–22. http://dx.doi.org/10.1139/o98-099.

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Osteoclasts are hematopoietic cells which play important roles in bone remodeling and resorption. They have phenotypic characteristics of the monocyte/macrophage lineages. In this review we first describe the phylogeny of osteoclasts. Osteoclast generation is closely linked to the presence of bone tissues. The formation of bone cavities in aquatic animals is underdeveloped, even though they have cells which have the potential to differentiate into osteoclasts. Next we describe recent advances in our understanding of osteoclastogenesis that have resulted from the identification of critical mole

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Chole, Richard A. "Osteoclasts in Chronic Otitis Media, Cholesteatoma, and Otosclerosis." Annals of Otology, Rhinology & Laryngology 97, no. 6 (1988): 661–66. http://dx.doi.org/10.1177/000348948809700615.

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Bone resorption and remodeling are characteristic of chronic otitis media with and without cholesteatoma and otosclerosis. The consequences of this remodeling process may be hearing loss, repeated infection, vestibular disturbance, or intracranial complications. Evidence of osteoclastic bone resorption was found in surgical specimens of 11 of 24 cases of cholesteatoma, two of three cases of chronic otitis media, and three of ten cases of otosclerotic stapes; all three spongiotic lesions had osteoclasts. With careful serial sectioning these cells are almost always multinucleate and have the typ

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Blair, H. C., S. L. Teitelbaum, L. E. Grosso, et al. "Extracellular-matrix degradation at acid pH. Avian osteoclast acid collagenase isolation and characterization." Biochemical Journal 290, no. 3 (1993): 873–84. http://dx.doi.org/10.1042/bj2900873.

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Osteoclasts degrade bone matrix, which is mainly type I collagen and hydroxyapatite, in an acidic extracellular compartment. Thus we reasoned that osteoclasts must produce an acid collagenase. We purified this enzyme, a 31 kDa protein, from avian osteoclast lysates (in 100 mM acetate/1 mM CHAPS/1 mM dithiothreitol, pH 4.4), fractionated by (NH2)2SO4 precipitation, gelatin-affinity, cation exchange, and gel filtration. Fraction activity was measured using diazotized collagen or 3H-labelled cross-linked collagen (decalcified and trypsin-treated metabolically L-[4,5-3H]proline-labelled bone) as s

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Wang, Qiang, Yi Xie, Quan-Sheng Du, et al. "Regulation of the formation of osteoclastic actin rings by proline-rich tyrosine kinase 2 interacting with gelsolin." Journal of Cell Biology 160, no. 4 (2003): 565–75. http://dx.doi.org/10.1083/jcb.200207036.

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Osteoclast activation is important for bone remodeling and is altered in multiple bone disorders. This process requires cell adhesion and extensive actin cytoskeletal reorganization. Proline-rich tyrosine kinase 2 (PYK2), a major cell adhesion–activated tyrosine kinase in osteoclasts, plays an important role in regulating this event. The mechanisms by which PYK2 regulates actin cytoskeletal organization and osteoclastic activation remain largely unknown. In this paper, we provide evidence that PYK2 directly interacts with gelsolin, an actin binding, severing, and capping protein essential for

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Abdel Razik, Heba E., Miho Nakamura, Leire Bergara-Muguruza, et al. "Osteoblast-Mediated Resorption of Porous Bioactive SCPC Granules Enhances Bone Regeneration in Human Extraction Sockets." Solid State Phenomena 340 (December 23, 2022): 107–12. http://dx.doi.org/10.4028/p-32eola.

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Bone graft materials are widely used in orthopedic and maxillofacial surgeries. The controlled resorbability of the graft material is essential for bone regeneration. Hydroxyapatite and biphasic calcium phosphate bone grafts have poor resorption and limited bone conductive effects. Histology analyses of bone biopsy from SCPC grafted human extraction sockets showed complete bone regeneration and graft resorption in absence of osteoclasts and macrophages. The hypothesis of the present study is that bioactive SCPC inhibits osteoclast’s activity due to the presence of resorbable silica phase in th

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Cackowski, Frank C., Judith L. Anderson, Kenneth D. Patrene, et al. "Osteoclasts are important for bone angiogenesis." Blood 115, no. 1 (2010): 140–49. http://dx.doi.org/10.1182/blood-2009-08-237628.

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Abstract Increased osteoclastogenesis and angiogenesis occur in physiologic and pathologic conditions. However, it is unclear if or how these processes are linked. To test the hypothesis that osteoclasts stimulate angiogenesis, we modulated osteoclast formation in fetal mouse metatarsal explants or in adult mice and determined the effect on angiogenesis. Suppression of osteoclast formation with osteoprotegerin dose-dependently inhibited angiogenesis and osteoclastogenesis in metatarsal explants. Conversely, treatment with parathyroid hormone related protein (PTHrP) increased explant angiogenes

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Fong, E. L. S., E. L. Prabha, and T. Carney. "POS0348 DEVELOPING A WHOLE MOUNT FLUORESCENT OSTEOCLAST ACTIVITY ASSAY USING THE ELF97 PHOSPHATASE SUBSTRATE TO VISUALISE AND QUANTIFY IN SITU OSTEOCLAST ACTIVITY IN ZEBRAFISH (DANIO RERIO)." Annals of the Rheumatic Diseases 81, Suppl 1 (2022): 427.3–428. http://dx.doi.org/10.1136/annrheumdis-2022-eular.5402.

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BackgroundOsteoporosis is a mineral bone disease arising from the predominance of osteoclastic bone resorption. Bisphosphonates which inhibit osteoclasts are commonly used in osteoporosis treatment, but are not without severe adverse effects like osteonecrosis of the jaw. The mechanisms behind the development of such phenomena is not well understood. Bone homeostasis is achieved through an intimate cross-talk between osteoclasts and osteoblasts. Thus, it is important to visualise activities of these cells simultaneously in situ. Currently, there are means to visualise osteoclast shape and numb

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Koyanagi, Yu, Eiko Sakai, Yu Yamaguchi, et al. "Dennd2c Negatively Controls Multinucleation and Differentiation in Osteoclasts by Regulating Actin Polymerization and Protrusion Formation." International Journal of Molecular Sciences 25, no. 21 (2024): 11479. http://dx.doi.org/10.3390/ijms252111479.

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Osteoclasts are bone-resorbing multinucleated giant cells formed by the fusion of monocyte/macrophage lineages. Various small GTPases are involved in the multinucleation and differentiation of osteoclasts. However, the roles of small GTPases regulatory molecules in osteoclast differentiation remain unclear. In the present study, we examined the role of Dennd2c, a putative guanine nucleotide exchange factor for Rab GTPases, in osteoclast differentiation. Knockdown of Dennd2c promoted osteoclast differentiation, resorption, and expression of osteoclast markers. Morphologically, Dennd2c knockdown

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Lee, B. S., L. S. Holliday, B. Ojikutu, I. Krits, and S. L. Gluck. "Osteoclasts express the B2 isoform of vacuolar H(+)-ATPase intracellularly and on their plasma membranes." American Journal of Physiology-Cell Physiology 270, no. 1 (1996): C382—C388. http://dx.doi.org/10.1152/ajpcell.1996.270.1.c382.

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Osteoclasts express high levels of vacuolar H(+)-ATPase (V-ATPase) in their ruffled membranes, driving the secretion of H+ required for normal bone resorption. Previous reports have suggested that the B subunit of the osteoclast V-ATPase differs from those expressed in kidney and other tissues. In this study, B subunit isoform-specific antibodies and cDNA probes were used to examine which B subunit isoform is expressed in osteoclasts and osteoclast-like cells. Immunoblotting and RNA hybridization analysis were used to demonstrate that cells from an osteoclast-rich mouse bone marrow culture mod

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Kolb, Alexus D., Jinlu Dai, Evan T. Keller, and Karen M. Bussard. "‘Educated’ Osteoblasts Reduce Osteoclastogenesis in a Bone-Tumor Mimetic Microenvironment." Cancers 13, no. 2 (2021): 263. http://dx.doi.org/10.3390/cancers13020263.

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Breast cancer (BC) metastases to bone disrupt the balance between osteoblasts and osteoclasts, leading to excessive bone resorption. We identified a novel subpopulation of osteoblasts with tumor-inhibitory properties, called educated osteoblasts (EOs). Here we sought to examine the effect of EOs on osteoclastogenesis during tumor progression. We hypothesized that EOs affect osteoclast development in the bone-tumor niche, leading to suppressed pre-osteoclast fusion and bone resorption. Conditioned media (CM) was analyzed for protein expression of osteoclast factors receptor activator of nuclear

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Leightner, Amanda C., Carina Mello Guimaraes Meyers, Michael D. Evans, Kim C. Mansky, Rajaram Gopalakrishnan, and Eric D. Jensen. "Regulation of Osteoclast Differentiation at Multiple Stages by Protein Kinase D Family Kinases." International Journal of Molecular Sciences 21, no. 3 (2020): 1056. http://dx.doi.org/10.3390/ijms21031056.

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Balanced osteoclast and osteoblast activity is necessary for skeletal health, whereas unbalanced osteoclast activity causes bone loss in many skeletal conditions. A better understanding of pathways that regulate osteoclast differentiation and activity is necessary for the development of new therapies to better manage bone resorption. The roles of Protein Kinase D (PKD) family of serine/threonine kinases in osteoclasts have not been well characterized. In this study we use immunofluorescence analysis to reveal that PKD2 and PKD3, the isoforms expressed in osteoclasts, are found in the nucleus a

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Chellaiah, M. A., N. Kizer, R. Biswas, et al. "Osteopontin Deficiency Produces Osteoclast Dysfunction Due to Reduced CD44 Surface Expression." Molecular Biology of the Cell 14, no. 1 (2003): 173–89. http://dx.doi.org/10.1091/mbc.e02-06-0354.

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Osteopontin (OPN) was expressed in murine wild-type osteoclasts, localized to the basolateral, clear zone, and ruffled border membranes, and deposited in the resorption pits during bone resorption. The lack of OPN secretion into the resorption bay of avian osteoclasts may be a component of their functional resorption deficiency in vitro. Osteoclasts deficient in OPN were hypomotile and exhibited decreased capacity for bone resorption in vitro. OPN stimulated CD44 expression on the osteoclast surface, and CD44 was shown to be required for osteoclast motility and bone resorption. Exogenous addit

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Robinson, Lisa J., Salvatore Mancarella, Irina L. Tourkova, John B. Barnett, Harry C. Blair, and Jonathan Soboloff. "Critical Role for the Calcium-Release Activated Calcium Channel Orai1 In RANKL-Stimulated Osteoclast Formation From Monocytic Cells." Blood 116, no. 21 (2010): 928. http://dx.doi.org/10.1182/blood.v116.21.928.928.

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Abstract Abstract 928 Calcium signals are major regulators of human osteoclast formation and function, and the molecular mechanisms underlying calcium effects are of interest as possible targets for pharmacologic regulation of bone resorption. IP3-receptor regulated release of calcium stores is linked to NFATc1 activation, which stimulates expression of key osteoclast genes in precursors, but the roles of other calcium channels in osteoclastogenesis are not clear. In particular, the identity of the channel(s) mediating extracellular calcium influx triggered by release of calcium stores remains

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Chen, Shi, Alexander Robling, Xiaohong Li, et al. "Hyperactivation of p21ras and PI3-K Cooperate To Alter Murine and Human NF1 Haploinsufficient Osteoclast Functions." Blood 108, no. 11 (2006): 675. http://dx.doi.org/10.1182/blood.v108.11.675.675.

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Abstract Neurofibromatosis type 1 (NF1) is a common genetic disorder caused by mutations of the NF1 tumor suppressor gene that functions as a GTPase activating protein for Ras. Though nullizygous loss of NF1 is associated with the development of malignancies, haploinsufficient phenotypes are now being increasingly recognized to alter cell fates and functions in a number of tissues resulting in nonmalignant disease manifestations. Bone manifestations, including skeletal dysplasias, scoliosis, and osteoporosis occur in 30–60% of all NF1 patients and osteoporosis is an increasingly recognized hea

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Frisch, Benjamin, John M. Ashton, Adam Olm-shipman, Lianping Xing, Craig T. Jordan, and Laura Calvi. "Reciprocal Synergistic Interactions of Leukemic Cells with Osteoclast Progenitors in the Bone Microenvironment." Blood 112, no. 11 (2008): 322. http://dx.doi.org/10.1182/blood.v112.11.322.322.

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Abstract The bone marrow provides an essential regulatory microenvironment for adult hematopoiesis, however the relationship between the bone marrow microenvironment and malignant hematopoiesis remains poorly understood. To investigate the interactions between leukemia and the bone marrow microenvironment we utilized a mouse model of blast-crisis chronic myelogenous leukemia (BC-CML), in which primitive normal murine hematopoietic cells are modified to leukemic cells by expressing the translocation products BCR/ABL and Nup98/HoxA9. The presence of each translocation was confirmed by their co-e

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Klein-Nulend, J., M. A. van Duin, T. P. Green, V. Everts, and T. J. de Vries. "The dual specific Src/Abl kinase inhibitor AZD0530 inhibits the formation and activity of human osteoclasts." Journal of Clinical Oncology 25, no. 18_suppl (2007): 3602. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.3602.

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3602 Background: Gene knockout studies have demonstrated the critical importance of the non-receptor TK Src to osteoclast bone resorptive function. Deregulated Src TK activity is also reported as a hallmark of the invasive cancer cell. Bone metastatic cancer cells interact with and activate osteoclasts in a destructive cycle of bone degradation and stimulation of tumor cell growth. Therefore targeting Src activity would appear to be a rational therapeutic approach in treating metastatic bone disease. We have reported previously (AACR 2005) on the activity of the dual Src/Abl kinase inhibitor A

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