Готові списки джерел за темами / Osteoclasts

Добірка наукової літератури з теми "Osteoclasts"

Автор: Grafiati
Опубліковано: 4 червня 2021
Оновлено: 10 березня 2023

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Статті в журналах з теми "Osteoclasts":

1

Combs, Charlotte E., Karen Fuller, Hashethra Kumar, Anthony P. Albert, Grisha Pirianov, James McCormick, Ian C. Locke, Timothy J. Chambers, and Kevin M. Lawrence. "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 (November 14, 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 10−7 M (P<0.001). UCN also inhibited osteoclast motility (10−7 M) but had no effect on osteoclast survival. Osteoclasts expressed mRNA encoding both UCN and the CRF receptor 2β subtype. Pre-osteoclasts however, expressed CRF receptor 2β alone. Unstimulated osteoclasts contained constitutively active cation channel currents with a unitary conductance of 3–4 pS, which were inhibited by over 70% with UCN (10−7 M). Compounds that regulate calcium signalling and energy status of the cell, both crucial for osteoclast activity were investigated. The non-selective cation channel blockers, lanthanum (La3+) and gadolinium (Gd3+), inhibited actin ring formation in osteoclasts, whereas modulators of voltage-dependent Ca2+ channels and KATP channels had no effect. These findings show for the first time that UCN is a novel anti-resorptive molecule that acts through a direct effect on osteoclasts and their precursor cells.
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 (November 1, 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 presence of vitamin D and analyzed the number of osteoclasts formed and the amount of TRAP 5b activity released into the culture medium. Results: TRAP 5b activity was not secreted from osteoclast precursor cells. Addition of clodronate-containing liposomes decreased in a dose-dependent manner the number of osteoclasts and TRAP 5b activity released in 6-day cultures. The amount of TRAP 5b activity in the medium detected by the immunoassay correlated significantly with the number of osteoclasts formed (r = 0.94; P &lt;0.0001; n = 120). Conclusions: The TRAP 5b immunoassay can be used to replace the laborious and time-consuming microscopic counting of osteoclasts in the osteoclast differentiation assay and to test the effects of potential therapeutic agents on osteoclast differentiation, enabling fast screening of large amounts of potential therapeutic agents.
3

Niida, Shumpei, Masato Kaku, Hitoshi Amano, Hisahiro Yoshida, Hiroshi Kataoka, Satomi Nishikawa, Kazuo Tanne, Norihiko Maeda, Shin-Ichi Nishikawa, and Hiroaki Kodama. "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 (July 19, 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 comparable to that of rhVEGF, showing that the VEGF signal is mediated through VEGFR-1. The rhM-CSF–induced osteoclasts died after injections of VEGFR-1/Fc chimeric protein, and its effect was abrogated by concomitant injections of rhM-CSF. Osteoclasts supported by rhM-CSF or endogenous VEGF showed no significant difference in the bone-resorbing activity. op/op mice undergo an age-related resolution of osteopetrosis accompanied by an increase in osteoclast number. Most of the osteoclasts disappeared after injections of anti-VEGF antibody, demonstrating that endogenously produced VEGF is responsible for the appearance of osteoclasts in the mutant mice. In addition, rhVEGF replaced rhM-CSF in the support of in vitro osteoclast differentiation. These results demonstrate that M-CSF and VEGF have overlapping functions in the support of osteoclastic bone resorption.
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 (June 1, 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 that while inhibition of cysteine proteinases strongly suppressed osteoclastic resorption, inhibitors of collagenase were without effect on the number, size, or demineralised fringe of excavations. We could find no evidence of expression of mRNA for collagenase in rat osteoclasts by in situ hybridisation, but found that it was expressed by chondrocytes, bone surface cells and osteocytes adjacent to osteoclasts. The distribution of these cells, and the correlation between increased collagenase production and increased stimulation of osteoclastic resorption in vitro by bone cells, suggests that these cells might be involved in the regulation of bone resorption in situ, and that collagenase production might play a role in this process.
5

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 (September 7, 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 activity, we tested its effects on mature osteoclasts. TRANCE rapidly induced a dramatic change in osteoclast motility and spreading and inhibited apoptosis. In populations of osteoclasts that were unresponsive to PTH, TRANCE caused activation of bone resorption equivalent to that induced by PTH in the presence of osteoblastic cells. Moreover, osteoblast-mediated stimulation of bone resorption was abrogated by soluble TRANCE receptor and by the soluble decoy receptor osteoprotegerin (OPG), and stimulation of isolated osteoclasts by TRANCE was neutralized by OPG. Thus, TRANCE expression by osteoblasts appears to be both necessary and sufficient for hormone-mediated activation of mature osteoclasts, and TRANCE-R is likely to be a receptor for signal transduction for activation of the osteoclast and its survival.
6

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 (1 березня 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 decoy receptor, suggesting that this was due to a direct action on osteoclasts. Bone resorption was similarly directly and potently stimulated, in a RANKL-independent manner in osteoclasts, whether these were formed in vitro or in vivo. Interestingly, TNFα promoted actin ring formation at concentrations an order of magnitude below those required for osteoclastic differentiation. Moreover, TNFα strongly synergized with RANKL, such that miniscule concentrations of TNFα were sufficient to substantially augment osteoclast activation. The extreme sensitivity of osteoclasts to activation by TNFα suggests that the most sensitive osteolytic response of bone to TNFα is through activation of existing osteoclasts; and the strong synergy with RANKL provides a mechanism whereby increased osteolysis can be achieved without disturbance to the underlying pattern of osteoclastic localization.
7

Yu, Anna Xiao-Dan, Jian Xiao, Shi-Zheng Zhao, Xiang-Peng Kong, Kenneth Kin-Leung Kwan, Brody Zhong-Yu Zheng, Kevin Qi-Yun Wu, Tina Ting-Xia Dong, and Karl Wah-Keung Tsim. "Biological Evaluation and Transcriptomic Analysis of Corylin as an Inhibitor of Osteoclast Differentiation." International Journal of Molecular Sciences 22, no. 7 (March 29, 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, and subsequently the expressions of osteoclastic proteins were suppressed: the suppression of protein expression was further illustrated by transcriptomic analysis. Furthermore, corylin inhibited the nuclear translocation of p65, giving rise to a restraint in osteoclastic differentiation through the attenuation of transcription factors nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and nuclear factor of activated T cells c1 (NFATc1). There was no obvious change in apoptosis when the RANKL-induce osteoclasts were cultured in the presence of corylin. The finding supports the potential development of corylin as an osteoclast inhibitor against osteoporosis.
8

Nakamura, I., M. F. Pilkington, P. T. Lakkakorpi, L. Lipfert, S. M. Sims, S. J. Dixon, G. A. Rodan, and L. T. Duong. "Role of alpha(v)beta(3) integrin in osteoclast migration and formation of the sealing zone." Journal of Cell Science 112, no. 22 (November 15, 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 cells formed in a co-culture system. We show that: (1) echistatin inhibits bone resorption in vitro at lower concentrations (IC(50)= 0.1 nM) than those required to detach osteoclasts from bone (IC(50) approximately 1 microM); (2) echistatin (IC(50)= 0.1 nM) inhibits M-CSF-induced migration and cell spreading of osteoclasts; (3) alpha(v)beta(3) integrins are localized in podosomes at the leading edge of migrating osteoclasts, whereas, with echistatin treatment (0.1 nM), alpha(v)beta(3) disperses randomly throughout the adhesion surface; and (4) when bone resorption is fully inhibited with echistatin, there is visible disruption of the sealing zone (IC(50)= 13 nM), and alpha(v)beta(3) visualized with confocal microscopy re-distributes from the basolateral membranes to intracellular vesicular structures. Taken together, these findings suggest that alpha(v)beta(3) integrin plays a role in the regulation of two processes required for effective osteoclastic bone resorption: cell migration (IC(50)= 0.1 nM) and maintenance of the sealing zone (IC(50) approximately 10 nM).
9

Kameda, Takashi, Hiroshi Mano, Tatsuhisa Yuasa, Yoshihisa Mori, Koshi Miyazawa, Miho Shiokawa, Yukiya Nakamaru, et al. "Estrogen Inhibits Bone Resorption by Directly Inducing Apoptosis of the Bone-resorbing Osteoclasts." Journal of Experimental Medicine 186, no. 4 (August 18, 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 and induction of osteoclast apoptosis. These data suggest that the protective effects of estrogen against postmenopausal osteoporosis are mediated in part by the direct induction of apoptosis of the bone-resorbing osteoclasts by an estrogen receptor– mediated mechanism.
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 (June 1, 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 bone, a pattern of inhibition previously observed in response to macrophage CSF (M-CSF). MIP-2, RANTES, MIP-1 beta, and monocyte chemotactic protein-1 were without effect on resorption. MIP-1 alpha and IL-8, but not the other chemokines, also stimulated osteoclastic motility and increased the osteoclast spread area in a dose-dependent manner, over the same concentration range as that which inhibited bone resorption. In addition, MIP-1 alpha induced osteoclast orientation in a gradient of the chemokine, and stimulated osteoclast migration. We detected no effect of chemokines on osteoclast formation or survival. Our data suggest that chemokines can promote osteoclast orientation and migration, processes that might be involved in chemotaxis; it seems appropriate that resorptive functions should be suppressed during migration. Because chemokines are proinflammatory, their actions on osteoclasts might represent mechanisms by which bone resorption is modulated by the inflammatory process when this occurs in bone. However, given that chemokines are increasingly recognized to be multifunctional and that they are produced by cells of the osteoblastic lineage, they may also be components of the physiologic regulation of bone resorption.
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Статті в журналах Дисертації Книги

Дисертації з теми "Osteoclasts":

1

O'Brien, Elizabeth Ann. "Regulation of osteoclast activity : differential adhesion of osteoclasts to the bone surface." Thesis, University of Liverpool, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343930.

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2

Rowlands, Marit-Naomi. "In vitro production of osteoclasts." Thesis, University of Liverpool, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250270.

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3

Nesbitt, Stephen Anthony. "Collagen binding proteins in osteoclasts." Thesis, Open University, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265344.

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4

Herrera, Bruno Schneider. "Óxido nítrico e periodontite experimental: caracterização de mediadores intracelulares da atividade osteoclastogênica, conseqüências locais e sistêmicas." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-11092008-154717/.

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A doença periodontal é a doença crônica mais prevalente nas doenças orais. Dentre os mediadores desse processo contam-se a Resolvina E1 (RvE1), um mediador pró-resolução da inflamação capaz de diminuir a perda óssea secundária á doença periodontal em coelhos, e o oxido nítrico (NO), o qual pode ser produzido em grandes quantidades pela ação de citocinas e estimular a diferenciação e atividade osteoclástica. O objetivo deste estudo foi investigar os efeitos da RvE1 em osteoclastos (OCs) em cultura e os mecanismos envolvidos, bem como o papel do NO na progressão da periodontite experimental em ratos e as alterações sistémicas resultantes de danos oxidativos. A diferenciação de OCs foi induzida em células de medula óssea de camundongos C57BL/6 em cultura (7 dias) e tratadas com diferentes doses de RvE1. NFkB e Akt fosforilada foram analisadas por Western blotting e a expressão gênica de NO sintase (NOS) induzível (iNOS) por \"real-time\" PCR. A participação dos receptores ChemR23 e BLT-1 na resposta à RvE1 foi estudada em membranas isoladas de OCs empregando radioligantes. A perda óssea alveolar e danos em órgãos periféricos foram analisados em ratos com periodontite induzida por ligadura (P) e sob tratamento de longo prazo com o inibidor não-seletivo de NOS, L-NAME. Os animais receberam L-NAME durante as 2 semanas prévias à indução da periodontite e até o momento do sacrifício (3, 7 ou 14 após a ligadura). A perda óssea alveolar foi avaliada radiograficamente, e análises do conteúdo de proteínas contendo nitrotirosina (NT), espécies reativas do ácido tiobarbitúrico (TBARs) e atividade da mieloperoxidase (MPO) foram realisadas em amostras de coração, baço, rim, fígado e pulmão. RvE1 (3 ng/mL) através da ativação do receptor para BLT-1 (mas não ChemR23) inibiu a diferenciação e atividade de OCs (p<0,05) após 5 ou 7 dias de cultura, assim como a fosforilação dos dois sítios da Akt e a traslocação do NF-kB para o núcleo, um evento chave tanto na diferenciação de OCs (p<0,05) como na diminuição da expressão de iNOS. In vivo, ratos P (dia 7) mostraram um aumento na expressão de NT cardíaca e MPO renal em comparação ao grupo Sham (S; p<0,05). L-NAME resultou em aumento de NT hepática no grupo P no dia 3 (p<0,05), mas diminuição da NT cardíaca no dia 7 (p<0,01). Em comparação ao grupo P, ratos P+LN mostraram um aumento significativo na MPO hepática, cardíaca e renal no dia 3 (p<0,05), mas diminuição de MPO (dia 7) e TBARs esplênico (dia 3, p<0,05). Em resumo, mostramos que a RvE1 ligando-se ao receptor para BLT-1 inibe a diferenciação e atividade de OCs interferindo com a sinalização de Akt e NF-kB, e consequentemente inibindo a expressão da iNOS, e que o NO tem um papel central na periodontite, não só relacionado a consequências locais na perda óssea alveolar, como também em órgãos periféricos distantes.
The periodontal disease is the most prevalent chronic disease in oral diseases. Among the mediators of this process, is the Resolvin E1 (RvE1), a novel mediator pro-resolving of inflammation that is capable to decrease alveolar bone loss secondary to periodontal disease in rabbits; and the nitric oxide (NO), that can be produced in large amount, induced by cytokines and it can stimulate the osteoclast differentiation and activity. The aim of this study is to investigate the effects of RvE1 on osteoclasts (OCs) culture and the pathway involved, also the role of NO in the progression of experimental periodontitis in rats and systemic alterations due to oxidative damage. The OCs differentiation was induced in bone marrow cell culture from C57BL/6 mice (7 days) and treated with various doses of RvE1. NFkB and Akt phosphorylation were analyzed with Western blotting and the genic expression of NO synthase (NOS) inducible (iNOS) with \"Real Time\" PCR. The role of receptors ChemR23 and BLT-1 was accessed in OCs isolated membranes performing radioligants. The alveolar bone loss and peripheral organ damage was assessed in rats with ligature-induced periodontitis (P) under a long-term treatment of a NOS inhibitor, L-NAME. The animals received L-NAME from two weeks prior to periodontitis induction and until their sacrifice (3, 7 and 14 days after ligature). The alveolar bone loss was evaluated radiographically, and the protein nitrotyrosine (NT) content, reactive species of thiobarbituric acid (TBARs) and myeloperoxidase activity (MPO) were analyzed in samples of heart, spleen, kidney, lungs and kidneys. RvE1 (3 ng/mL) trough BLT-1 receptor activation (but not ChemR23) inhibits the OCs differentiation and activity (p<0.05) after 5 or 7 days of the culture, as well as the Akt phosphorylation and NF-kB translocation to the nucleus, a key event both in OCs differentiation (p<0.05) and iNOS expression decreases. In vivo, P rats (day 7) show an increase of heart NT and renal MPO, but lower lung MPO activity in comparison to the Sham group (S; p<0.05). L-NAME leads to an increase the liver NT expression in P rats on day 3 (p<0.05), but decreases the cardiac NT on day 7 (p<0.01). In comparison with the P group, P+LN rats showed significantly increased liver, heart and kidney MPO content on day 3 (p<0.05), but lower lung MPO (day 7) and spleen TBARs (day 3) content (p<0.05). In summary we have shown that RvE1 binding on BLT-1 receptor inhibits OCs differentiation and activity by interfering with Akt and NF-kB signaling and consequently iNOS inhibition, and NO has a central role on periodontitis, not only related to the local consequences on alveolar bone resorption, but also on distant peripheral organs.
5

Taylor, Adam. "The role of Rab GTPases in osteoclasts." Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2009. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=59017.

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6

Hussein, Osama. "Interaction of breast cancer cells with osteoclasts." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103695.

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Анотація:
Breast cancer is a major health problem. Metastatic disease is generally incurable. In the majority of patients, the skeleton bears the major metastatic burden. Bony lesions of metastatic breast cancer are usually osteolytic. Osteolytic metastases are formed by the pathological activation of osteoclasts. Anti-osteoclastic drugs are standard of care for patients suffering from breast cancer metastases. We conducted this project to decipher the signalling mechanisms responsible for osteoclasts activation in response to exposure to mediators released from mammary carcinoma cells. We evaluated the apoptotic profiles of osteoclasts in vitro in the presence of soluble factors derived from mammary carcinoma cells cultures. We observed a significant inhibition of osteoclasts apoptosis secondary to exposure to breast cancer cells-derived factors. This effect was not reversed with bisphosphonates. The pro-apoptotic protein BIM in osteoclasts was a target of modulation by breast cancer cells-derived factors. We proceeded to characterize the osteoclasts intracellular signalling pathways modulated by mammary carcinoma cells-derived factors. We identified phospholipase C γ (PLC γ) and the mammalian target of rapamycin (mTOR) as mechanistic meditors of the anti-apoptotic effect of cancer cells on osteoclasts. We tested the therapeutic benefit of rapamycin administration in a mouse model of experimental bone metastases of mammary carcinoma. In this model, rapamycin therapy inhibited metastasis-associated osteolysis, prolonged animal survival and reversed some tumour-induced immune changes in the host. Taken together, these studies provide new insights into the pathophysiology of breast cancer metastasis to bone, and demonstrate that targeting osteoclast signalling mediators, such as mTOR provides therapeutic benefits in experimental bone metastasis model.
Le cancer du sein est un problème de santé important. La maladie métastatique est généralement incurable. Dans la majorité de patients, le squelette soutient le fardeau métastatique principal. Les lésions osseuses du cancer du sein métastatique sont habituellement ostéolytique. Des métastases ostéolytique sont constituées par l'activation pathologique des osteoclasts. Les drogues anti-osteoclastiques sont mesures de soin essentiales pour des patients souffrant des métastases de cancer du sein. Nous avons conduit ce projet pour déchiffrer les mécanismes de signalisation responsables de l'activation d'osteoclasts en réponse à l'exposition aux médiateurs libérés des cellules mammaires de carcinome. Nous avons évalué les profils apoptotiques des osteoclasts in vitro en présence des facteurs solubles dérivés des cultures mammaires de cellules de carcinome. Nous avons observé une inhibition significative d'apoptosis d'osteoclasts secondaire à l'exposition aux facteurs cellule-dérivés par cancer du sein. Cet effet n'a pas été renversé avec des bisphosphonates. La pro-apoptotic protéine BIM dans les osteoclasts était une cible de la modulation par des facteurs cellule-dérivés par cancer du sein. Nous avons procédé caractériser les voies de signalisation intracellulaires d'osteoclasts modulées par des facteurs cellule-dérivés par carcinome mammaire. Nous avons identifié la phospholipase C (PLC γ) et la cible mammifère du rapamycin (mTOR) en tant que meditors mécanistes de l'effet anti-apoptotic des cellules de cancer sur des osteoclasts. Nous avons examiné l'avantage thérapeutique de l'administration de rapamycin dans un modèle de souris des métastases expérimentales d'os du carcinome mammaire. Dans ce modèle, la thérapie de rapamycin a empêché l'osteolysis métastase-associé, a affecté des survies animales prolongée et renversé quelques changements immunisés induits par la tumeur.
7

Gray, A. "Isolation, generation and characterization of equine osteoclasts." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.599624.

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a) Equine osteoclasts (OCs) were identified in ex vivo samples of developing long bone. They were particularly numerous in areas of active bone formation and remodelling such as at the longitudinal septum between cartilage and subchondral bone and in the spongiosum. Equine OCs were identified as being typically multinuclear and expressing very high levels of tartrate resistant acid phosphatase (TRAP) and cathepsin K. Only low levels of cathepsin B were detected in equine OCs. b) Techniques were developed to isolate equine OCs for the first time in vitro. The phenotype of these cells was clearly defined; they were multinuclear, expressed TRAP, the vitronectin receptor (VNR) and were observed in direct association with areas of resorption when cultured on ivory slices. However, equine OCs could only be isolated in small numbers in vitro and were often of poor viability. c) Techniques were developed to generate equine osteoclast-like cells (OCLs) for the first time in vitro from bone marrow cells (BMCs) with or without osteoblastic support cells. d) Equine OCLs demonstrated high levels of cathepsin K activity but only low levels of cathepsin B activity as determined by the use of fluorogenic substrates for these enzymes. e) The bisphosphonate pamidronate (APD) caused a dose-dependent inhibition of resorption by equine OCLs. APD also dose-dependently reduced the number of OCLs present in MNCEP cultures after 7d incubation but paradoxically increased the resorption undertaken by similar cultures at certain concentrations. f) Calcitonin inhibited resorption by equine OCLs apparently by inducing cytoplasmic retraction. g) Resorption by OCLs was also inhibited by insulin and the proton-pump inhibitor, bafilomycin.
8

Franco, Gilson Cesar Nobre. "Analise da farmacocinetica e dos indices PK/PD da doxiciclina no plasma, fluido gengival e saliva e avaliação de seu efeito sobre a osteoclastogenese mediada por RANKL." [s.n.], 2007. http://repositorio.unicamp.br/jspui/handle/REPOSIP/288516.

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Анотація:
Orientadores: Pedro Luiz Rosalen, Francisco Carlos Groppo, Toshihisa Kawai
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba
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Resumo: Doxiciclina (Dox) é um antimicrobiano pertencente à família das tetraciclinas com um amplo espectro de ação contra bactérias Gram-positivas e Gram-negativas. Além de suas propriedades antimicrobianas, Dox é atualmente empregada na periodontia como um modulador da resposta do hospedeiro (MRH), ao inibir a atividade da enzima metaloproteinase de matriz (MMP), a qual está relacionada ao processo de destruição tecidual. Neste contexto, este trabalho teve os seguintes objetivos: 1-determinar os parâmetros farmacocinéticos e integrar os índices PK/PD da Dox para o plasma, fluido gengival (FG) e saliva; 2-analisar os efeitos in vitro e in vivo da Dox sobre a osteoclastogênese com a finalidade de elucidar possíveis propriedades biológicas adicionais deste fármaco como MRH. Para a análise farmacocinética, 12 voluntários receberam dose oral única de 100 mg de Dox. Sangue, FG e saliva foram coletados em tempos pré-determinados e a concentração da Dox nestes fluidos foi determinada por bioensaio. A análise dos principais índices PK/PD da Dox foi realizada considerando o CIM para P. gingivalis. Para o segundo objetivo, o efeito da Dox sobre os processos de diferenciação e ativação osteoclástica foi verificado, respectivamente, pela contagem de células TRAP+ multinucleadas geradas a partir de células precursoras estimuladas com sRANKL na presença ou ausência de Dox e pela análise das lacunas de reabsorção formadas por estas células, quando cultivadas sobre discos de dentina. In vivo, o efeito da Dox sobre a osteoclastogênese foi determinado através da indução deste processo em calvária de camundongo. Solução de sRANKL/LPS foi injetada na região da calvária e os animais receberam, por gavagem, Dox ou placebo diariamente. Após 10 dias, a calvária foi removida para análise histoquímica. Em acréscimo, a atividade da Dox sobre a expressão de genes responsáveis pelos processos de diferenciação e ativação osteoclástica foi analisada por RT-PCR. Durante os experimentos in vitro e in vivo, a produção e atividade da MMP foram verificadas através de Western-blot e Zimograma respectivamente. Os resultados demonstraram que as maiores concentrações de Dox foram observadas no plasma, seguido pelo FG e saliva. A análise dos índices PK/PD da Dox indicou que a dose de 100 mg foi insuficiente para se obter os valores ideais antimicrobianos preconizados na /CIM. Os experimentos in vitro e in vivo sobre o efeito da Dox como MRH demonstraram que este fármaco inibiu os processos de diferenciação e ativação dos osteoclastos. Dox também modulou a expressão de proteínas diretamente relacionadas a osteoclastogênese, incluindo TRAP, Catepsina K e c-Myc. Finalmente, embora a síntese da MMP não tenha sido afetada, a atividade da MMP foi reduzida na presença de Dox. Portanto, os resultados do presente estudo sugerem que uma dose inicial maior do que 100 mg é necessária para alcançar o valor preconizado para ASC/CIM e Cmax/CIM, com a finalidade de se obter os melhores resultados clínicos antimicrobianos. A análise da Dox como MRH indicou que este fármaco pode atuar neste processo não somente pela sua capacidade de inativar a MMP, e sim, por apresentar a propriedade de inibir a diferenciação e ativação osteoclástica, incluindo a modulação de sua expressão gênica. literatura para os parâmetros ASC/CIM e Cmax
Abstract: Doxycycline (Dox), a member of the tetracycline family, is an antimicrobial agent with a broad-spectrum of activity against Gram-positive and Gram-negative bacteria. In addition to its antimicrobial properties, Dox is used in the treatment of periodontal diseases as a host response modulator by inhibiting the activity of an important enzyme, matrix metalloproteinase (MMP), which is related to the process of tissue destruction. In this context, this study had the following aims: 1-to determine the pharmacokinetic parameters of Dox and to integrate the PK/PD indices for plasma, gingival crevicular fluid (GCF) and saliva; 2-to analyze the effects in vitro and in vivo of Dox on the osteoclastogenesis and on the osteoclast activation in order to elucidate additional biological properties of Dox on the host response modulation (HRM). Twelve volunteers received single oral administration of Dox (100 mg). Blood, GCF and saliva were collected and the concentrations were measured by bioassay technique. The PK/PD analyses were carried out using the MIC for P. gingivalis. For the second objective, the effect of Dox on the osteoclast differentiation and activation processes was determined, respectively, by the counting of TRAP+ multinuclear cells derived from osteoclast precursory cells sRANKL-stimulated in the presence or absence of Dox and by the analysis of the resorption areas formed by these cells when cultured on dentin discs. In vivo, Dox¿s effect on the osteoclastogenesis was verified using the model of osteoclastogenesis induction in mouse calvaria. sRANKL/LPS was injected in the supra-calvaria area and the animals received Dox or placebo daily by gavage. After the experimental period of 10 days, the calvariae were removed for histochemistry analyses. In addition, the effect of Dox on the expression of genes related to the osteoclast differentiation and activation processes was carried out using RT-PCR technique. MMP production and activity were ensured during in vitro and in vivo experiments by Western-blot and Zymography, respectively. The results demonstrated that Dox achieved the highest concentration in the plasma, following by GCF and saliva. PK/PD analyses showed that the dose of 100 mg was insufficient to get the antimicrobial levels indicated in the literature for AUC/MIC and Cmax/MIC indices. In vitro and in vivo studies of Dox¿s effects on the HRM demonstrated that this drug could inhibit the osteoclast differentiation and activation process. Dox also showed an important property of down-regulation in the expression of proteins directly related to osteoclastogenesis, including TRAP, Cathepsin K and c-Myc. Finally, although Dox did not affect the expression of MMP protein, MMP activity was remarkably decreased by Dox. Therefore, the present study suggests that higher doses than 100 mg would be necessary to obtain effective antimicrobial levels and the effect of DOX on the HRM can be due to not only by MMP inhibition but also by the direct effect on RANKL-mediated osteoclast differentiation and activation, including its gene regulation
Doutorado
Farmacologia, Anestesiologia e Terapeutica
Doutor em Odontologia
9

Cayana, Ezymar Gomes. "Efeito da administração intermitente do PTH (1-34) na periodontite experimental em ratas expostas à fumaça de cigarros." [s.n.], 2010. http://repositorio.unicamp.br/jspui/handle/REPOSIP/290845.

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Анотація:
Orientadores: Enilson Antônio Sallum, João Baptista César Neto
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba
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Resumo: O objetivo deste estudo foi investigar histológica e histoquimicamente a influência da inalação da fumaça de cigarros (IFC) e da administração intermitente de PTH 1-34 sobre a perda óssea alveolar na região de furca em ratas submetidas a periodontite experimental induzida por meio de ligaduras. Animais foram aleatoriamente distribuídos nos grupos: 1 - placebo (veículo) controle (n=11); 2- IFC + placebo (n=15); 3- PTH 1-34 (n=10); 4 - IFC + PTH 1-34 (n=15). Dentes controlaterais, não receberam ligaduras e serviram como controle. Após 60 dias com ligaduras, os animais foram sacrificados. A avaliação histométrica foi realizada quantificando a área de perda óssea na região da bifurcação e a análise histoquímica por meio de reação de fosfatase ácida tártarato resistente (TRAP). Os dados coletados foram analisados estatisticamente utilizando a análise de variância ANOVA e o teste Tukey (=5%). Nos dentes com ligaduras, uma análise intergrupo revelou aumento estatisticamente significante da perda óssea como resultado do modelo de periodontite induzida quando o grupo 2 foi comparado com os grupos 1, 3 e 4 respectivamente (p<0,05). O número de células marcadas positivamente pelo TRAP na superfície linear da crista óssea demonstrou um aumento significativo no número de osteoclastos para o grupo 2 quando comparado com os grupos 1, 3 e 4, respectivamente (P<0,05). Dentro dos limites do presente estudo, pode-se concluir que o PTH 1-34 na ausência ou presença de IFC pode reduzir significativamente a perda óssea resultante da periodontite experimental induzida por ligaduras
Abstract: The aim of the present investigation was to histologically and histoquimically evaluate, in an animal model (rats), the influence of cigarette smoke inhalation (CSI) and intermittent administration of PTH in rodents would block the alveolar bone loss when a ligature-induced periodontitis is used. Animals were randomly assigned in groups: 1 - placebo (vehicle) Control-ligated (n=11); 2 - CSI + placebo- ligated (n=15); 3 - PTH-treated ligated (n=10); 4 - CSI + PTH-treated ligated (n=15). Contralateral teeth were unligated to serve as controls. After 60 days with ligatures, the animals were killed. The histometric avaluete determined the area between the bone crest and cementum surface in the furcation regions of teeth and the number of cells positive for tartrate-resistant acid phosphatase (TRAP). The date were statistically analysed using ANOVA and Tukey's test (alpha=5%). At the ligated sites, intergroup analysis revealed significantly increased the bone loss resulting from ligature-induced periodontitis when group 2 compared with group 1, 3 and 4, respectively (P<0,05). The number of TRAP-Positive cell in the linear surface of the bone crest showed an increase for the group 2 compared with the group 1, 3 and 4, respectively (P<0,05). Whithin the limits of the present study, it can be concluded that PTH in the absence or presence of CSI may be minimize significantly the bone resorption associated with periodontitis
Doutorado
Periodontia
Doutor em Clínica Odontológica
10

Ford, Lorna. "An investigation into the effects of endocannabinoids and the COX-2 metabolite of 2-Arachidonyl glycerol on bone cells." Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2009. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=33596.

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Книги з теми "Osteoclasts":

1

R, Rifkin Barry, and Gay Carol V, eds. Biology and physiology of the osteoclast. Boca Raton: CRC Press, 1992.

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2

Yu, Hesheng. P2 purinoceptor-linked Ca2+ signaling and pH changes in osteoclasts. [Toronto: University of Toronto, Faculty of Dentistry], 1996.

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3

Felix, Bronner, Farach-Carson Mary C. 1958-, and Rubin Janet, eds. Bone resorption. London: Springer, 2005.

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4

Rodionova, N. V. Funkt͡s︡ionalʹnai͡a︡ morfologii͡a︡ kletok v osteogeneze. Kiev: Nauk. dumka, 1989.

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5

National Institute on Aging/National Institute of Dental Research Workshop on Human Models of Skeletal Aging (1994 Washington, D.C.). National Institute on Aging/National Institute of Dental Research Workshop on Human Models of Skeletal Aging: Washington, DC, March 1-2, 1994. Edited by Robey Pamela Gehron 1952-, Sherman Sherry, National Institute of Dental Research (U.S.), and National Institute on Aging. New York, NY: Springer International, 1995.

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6

Maria, Bijvoet Olav Leonardus, Lipton Allan, and International Cancer Congress (15th : 1990 : Hamburg, Germany), eds. Osteoclast inhibition in the management of malignancy-related bone disorders: An international symposium held during the 15th International Cancer Congress, Hamburg, Germany, August 1990. Seattle: Hogrefe & Huber, 1993.

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7

D, Rubens R., and European Conference on Clinical Oncology (5th : 1989 : London, England), eds. The Management of bone metastases and hypercalcaemia by osteoclast inhibition: An international symposium held during the 5th European Conference on Clinical Oncology (ECCO 5), London, September 1989. Toronto: Hogrefe & Huber, 1990.

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8

Shorey, Seema. Differences in the degree to which osteoclasts from different parts of the skeleton employ cathepsin K and matrix metalloproteinases for bone resorption. Ottawa: National Library of Canada, 2002.

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9

Holt, Ian. Control of osteoclast activity. Manchester: University of Manchester, 1996.

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10

David, Evered, Harnett Sara, and Ciba Foundation, eds. Cell and molecular biology of vertebrate hard tissues. Chichester, UK: Wiley, 1988.

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Частини книг з теми "Osteoclasts":

1

Baak, Marleen A., Bernard Gutin, Kim A. Krawczewski Carhuatanta, Stephen C. Woods, Heinz W. Harbach, Megan M. Wenner, Nina S. Stachenfeld, et al. "Osteoclasts." In Encyclopedia of Exercise Medicine in Health and Disease, 672. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2794.

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2

Crockett, Julie C., David J. Mellis, and Adam Taylor. "Transfection of Osteoclasts and Osteoclast Precursors." In Methods in Molecular Biology, 205–22. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-415-5_14.

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3

Roodman, G. David, Linda M. McManus, and Anne Demulder. "Pagetic Osteoclasts." In Medical Intelligence Unit, 45–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-22505-9_3.

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4

Győri, Dávid, and Attila Mócsai. "Osteoclasts in Inflammation." In Compendium of Inflammatory Diseases, 1047–53. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_155.

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5

Győri, Dávid, and Attila Mócsai. "Osteoclasts in Inflammation." In Encyclopedia of Inflammatory Diseases, 1–7. Basel: Springer Basel, 2013. http://dx.doi.org/10.1007/978-3-0348-0620-6_155-1.

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6

Atkins, Samantha K., Farwah Iqbal, Johana Barrientos, Cecilia Giachelli, and Elena Aikawa. "Osteoclasts in Cardiovascular Calcification." In Contemporary Cardiology, 391–419. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-46725-8_18.

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7

Rucci, Nadia, and Anna Teti. "Osteoclasts: Essentials and Methods." In Principles of Bone and Joint Research, 33–53. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-58955-8_3.

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8

Takahashi, Naoyuki, Nobuyuki Udagawa, Yasuhiro Kobayashi, and Tatsuo Suda. "Generation of Osteoclasts In Vitro, and Assay of Osteoclast Activity." In Arthritis Research, 285–301. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-401-8_18.

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9

Udagawa, Nobuyuki, Teruhito Yamashita, Yasuhiro Kobayashi, and Naoyuki Takahashi. "Identification of Osteoclasts in Culture." In Methods in Molecular Biology, 273–84. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-962-8_18.

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10

Rucci, Nadia, Alberta Zallone, and Anna Teti. "Isolation and Generation of Osteoclasts." In Methods in Molecular Biology, 3–19. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8997-3_1.

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Тези доповідей конференцій з теми "Osteoclasts":

1

Suzuki, Keiko, Baoqian Zhu, Harvey A. Goldberg, Susan R. Rittling, David T. Denhardt, Christopher A. G. McCulloch, and Jaro Sodek. "INTRACELLULAR OSTEOPONTIN IN OSTEOCLASTS: IMPAIRED MIGRATION, CELL FUSION AND RESORPTION IN OSTEOCLASTS FROM OPN-/- AND CD44-/- MICE." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.263.

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2

LI, Xiaojuan, Xiaorui XIE, Jin REN, Liling REN, and Jian CAO. "Effects of Propranolol on Osteoclasts Cultured in Vitro." In International Conference on Biological Engineering and Pharmacy 2016 (BEP 2016). Paris, France: Atlantis Press, 2017. http://dx.doi.org/10.2991/bep-16.2017.6.

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3

Brunner, Julia S., Melanie Hofmann, Victoria Saferding, Andrea Vogel, Birgit Niederreiter, Hannah Paar, Li Chen, Paul Cheng, Gernot Schabbauer, and Stephan Blüml. "02.28 The role of arginase I in osteoclasts." In 37th European Workshop for Rheumatology Research 2–4 March 2017 Athens, Greece. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2016-211050.28.

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4

Nemoto, Atsuko, Toshimasa Uemura, Takashi Ushida, and Tetsuya Tateishi. "GRAVITY EFFECTS ON mRNA EXPRESSION OF MARKER ENZYMES IN OSTEOCLASTS." In Proceedings of the 12th International Symposium on Ceramics in Medicine. WORLD SCIENTIFIC, 1999. http://dx.doi.org/10.1142/9789814291064_0065.

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5

Muraoka, Sei, Kaichi Kaneko, Natsuko Kusunoki, Shinichi Kawai, and Toshihiro Nanki. "THU0046 FRACTALKINE PROMOTES DIFFERENTIATION INTO OSTEOCLASTS FROM HUMAN PERIPHERAL BLOOD MONOCYTES." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.3046.

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6

Chen, Show-Huie, Chia-Ching Wu, Shyh-Hau Wang, and Weng-Tyng Li. "The inhibition effect of low-intensity pulsed ultrasound on osteoclasts progenitor cells." In 2012 IEEE International Ultrasonics Symposium. IEEE, 2012. http://dx.doi.org/10.1109/ultsym.2012.0151.

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7

Molhoek, AK, RE Li, ID Jansen, T. Schoenmaker, TJ de Vries, SJ van Vliet, and Y. van Kooyk. "P031/O12 Sialic acids negatively affect the bone resorptive capacity of osteoclasts." In 39th European Workshop for Rheumatology Research, 28 February–2 March 2019, Lyon, France. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2019.23.

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8

Huang, Junchi, Jan-Erik Damber, and Karin Welen. "Abstract B076: Osteoclasts influence androgen-related gene expression in prostate cancer cells." In Abstracts: AACR Special Conference: Prostate Cancer: Advances in Basic, Translational, and Clinical Research; December 2-5, 2017; Orlando, Florida. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.prca2017-b076.

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9

Yun Zhang, Cuiping Mao, Weimin Yan, and Xiaoxiang Zheng. "Application of cell engineering of herbal Medicine treating bone resorption of osteoclasts." In 2005 IEEE Engineering in Medicine and Biology 27th Annual Conference. IEEE, 2005. http://dx.doi.org/10.1109/iembs.2005.1615587.

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10

Penninger, Charles L., Ryan K. Roeder, Glen L. Niebur, and John E. Renaud. "Investigation of Osteoclast Resorption Mechanisms in a Hybrid Cellular Automaton Model of Bone Remodeling." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176171.

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Анотація:
Bone is a living tissue which is continually adapting to its biological environment via continuous formation and resorption. It is generally accepted that bone remodeling occurs in response to daily mechanical loading. The remodeling process enables various functions, such as damage repair, adaptation to mechanical loads, and mineral homeostasis [1]. The cells that are responsible for the bone remodeling process are the bone resorbing osteoclasts and the bone forming osteoblasts. These cells closely coordinate their actions in a basic multicellular unit to renew “packets” of bone.

Звіти організацій з теми "Osteoclasts":

1

Giachelli, Cecilia, Bruce Sangeorzan, Susan Lund, Steven Bain, Cameron Rementer, and Dewayne Threet. Engineered Osteoclasts for the Treatment and Prevention of Heterotopic Ossification. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada612445.

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2

Alikhani, Mani, Sarah Alansari, Mohammed Al Jearah, Niraj Gadhavi, Mohammad Hamidaddin, Fadwa Shembesh, Chinapa Sangsuwon, Jeanne Nervina, and Cristina Teixeira. Osteoclasts: The Biological Knife In Sutural Responses To Mechanical Stimulation. CTOR Press, May 2018. http://dx.doi.org/10.30771/2018.2.

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3

Alikhani, Mani, Sarah Alansari, Mohammed Al Jearah, Niraj Gadhavi, Mohammad Hamidaddin, Fadwa Shembesh, Chinapa Sangsuwon, Jeanne Nervina, and Cristina Teixeira. Osteoclasts: The biological knife in sutural responses to mechanical stimulation. CTOR Press, April 2018. http://dx.doi.org/10.30771/2018.3.

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4

Reddy, Sakamuri. Osteoclast Inhibitory Peptide-1 Therapy for Paget's Disease. Fort Belvoir, VA: Defense Technical Information Center, August 2010. http://dx.doi.org/10.21236/ada539193.

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5

Reddy, Sakamuri V. Osteoclast Inhibitory Peptide-1 Therapy for Paget's Disease. Fort Belvoir, VA: Defense Technical Information Center, August 2012. http://dx.doi.org/10.21236/ada567774.

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6

Reddy, Sakamuri. Osteoclast Inhibitory Peptide-1 Therapy for Paget's Disease. Fort Belvoir, VA: Defense Technical Information Center, August 2011. http://dx.doi.org/10.21236/ada553287.

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7

Reddy, Sakamuri V. Measles Virus Nucleocapsid (MJVNP) Gene Expression and RANK Receptor Signaling in Osteoclast Precursors. Osteoclast Inhibitors Peptide Therapy for Pagets Disease. Fort Belvoir, VA: Defense Technical Information Center, October 2005. http://dx.doi.org/10.21236/ada484715.

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8

Reddy, Sakamuri V. Measles Virus Nucleocapsid (MVNP) Gene Expression and RANK Receptor Signaling in Osteoclast Precursors, Osteoclast Inhibitors Peptide Therapy for Pagets Disease. Fort Belvoir, VA: Defense Technical Information Center, October 2008. http://dx.doi.org/10.21236/ada500887.

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9

Reddy, Sakamuri V. Measles Virus Nucleocapsid (MVNP) Gene Expression and RANK Receptor Signaling in Osteoclast Precursors, Osteoclast Inhibitors Peptide Therapy for Pagets Disease. Fort Belvoir, VA: Defense Technical Information Center, October 2006. http://dx.doi.org/10.21236/ada462833.

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10

Reddy, Sakamuri V. Measles Virus Nucleocapsid (MVNP) Gene Expression and RANK Receptor Signaling in Osteoclast Precursors,Osteoclast Inhibitors Peptide Therapy for Pagets Disease. Fort Belvoir, VA: Defense Technical Information Center, October 2004. http://dx.doi.org/10.21236/ada482539.

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