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Bone Resorption

The Experts below are selected from a list of 234 Experts worldwide ranked by ideXlab platform

M. Schaueblin – 1st expert on this subject based on the ideXlab platform

  • TAXOL INHIBITS OSTEOCLASTIC Bone Resorption
    Calcified Tissue International, 1995
    Co-Authors: T.j. Hall, H. Jeker, M. Schaueblin

    Abstract:

    We have examined the effect of the anti-tumor compound taxol, on osteoclastic Bone Resorption. In the Bone slice assay, taxol (0.1–0.001 μM) dose-dependently inhibited Bone Resorption with an IC50 of 0.08 μM. Osteoclast survival on Bone slices was unaffected by 0.01–1 μM taxol, but 10 μ M was cytotoxic. Taxol (1 μM) also ihibited osteoclast spreading (45%) on fibronectin-coated slides. The antiproliterative effects of taxol are due to its unique ability to stabilize microtubules. Primary osteoclasts are nonproliferating end cells, so taxol probably inhibits Bone Resorption by intertering with other microtubule-dependent functions such as cell polarization, motility or vesicle exocytosis. Since these inhibitory effects on osteoclasts in vitro are seen with therapeutically relevant concentrations, taxol therapy may have beneficial side-effects e.g. inhibition of hyperealcemia and Bone metastases.

  • Taxol inhibits osteoclastic Bone Resorption
    Calcified Tissue International, 1995
    Co-Authors: T.j. Hall, H. Jeker, M. Schaueblin

    Abstract:

    We have examined the effect of the anti-tumor compound taxol, on osteoclastic Bone Resorption. In the Bone slice assay, taxol (0.1-0.001 microM) dose-dependently inhibited Bone Resorption with an IC50 of 0.08 microM. Osteoclast survival on Bone slices was unaffected by 0.01-1 microM taxol, but 10 microM was cytotoxic. Taxol (1 microM) also inhibited osteoclast spreading (45%) on fibronectin-coated slides. The antiproliferative effects of taxol are due to its unique ability to stabilize microtubules. Primary osteoclasts are nonproliferating end cells, so taxol probably inhibits Bone Resorption by interfering with other microtubule-dependent functions such as cell polarization, motility or vesicle exocytosis. Since these inhibitory effects on osteoclasts in vitro are seen with therapeutically relevant concentrations, taxol therapy may have beneficial side-effects e.g. inhibition of hypercalcemia and Bone metastases.

T.j. Hall – 2nd expert on this subject based on the ideXlab platform

  • TAXOL INHIBITS OSTEOCLASTIC Bone Resorption
    Calcified Tissue International, 1995
    Co-Authors: T.j. Hall, H. Jeker, M. Schaueblin

    Abstract:

    We have examined the effect of the anti-tumor compound taxol, on osteoclastic Bone Resorption. In the Bone slice assay, taxol (0.1–0.001 μM) dose-dependently inhibited Bone Resorption with an IC50 of 0.08 μM. Osteoclast survival on Bone slices was unaffected by 0.01–1 μM taxol, but 10 μ M was cytotoxic. Taxol (1 μM) also ihibited osteoclast spreading (45%) on fibronectin-coated slides. The antiproliterative effects of taxol are due to its unique ability to stabilize microtubules. Primary osteoclasts are nonproliferating end cells, so taxol probably inhibits Bone Resorption by intertering with other microtubule-dependent functions such as cell polarization, motility or vesicle exocytosis. Since these inhibitory effects on osteoclasts in vitro are seen with therapeutically relevant concentrations, taxol therapy may have beneficial side-effects e.g. inhibition of hyperealcemia and Bone metastases.

  • The role of reactive oxygen intermediates in osteoclastic Bone Resorption.
    Biochemical and Biophysical Research Communications, 1995
    Co-Authors: T.j. Hall, H. Jeker, M. Schaeublin, K. Fuller, T J Chambers

    Abstract:

    Abstract Osteoclasts have been shown to produce reactive oxygen intermediates (ROI) and it has been suggested that ROI are involved in the process of Bone Resorption. ROI have also been shown to play a central role in the activation of the multisubunit transcription factor NF-κB that enhances the transcription of genes encoding defence and signaling proteins. Therefore, we have assessed the effect of pyrrolidine dithiocarbamate (PDTC), an oxygen-radical scavenger and metal chelator that is a selective and potent inhibitor of NF-κB activation, on osteoclastic Bone Resorption in the Bone slice assay. PDTC (0.001 – 0.1 mM) dose-dependently and non-cytotoxically inhibited osteoclast activity with an IC 50 of 0.01 mM. PDTC (0.01 mM) caused no change in the ratio of Resorption pit area to Resorption pit depth as measured by Lasertec confocal microscopy, indicating that ROI are not involved in the resorptive process per se . This view is supported by time-course studies showing that addition of PDTC or N-acetyl cysteine (NAG; an ROI scavenger, but not metal chelator), 6 hr after the start of the assay had no significant effect on subsequent Bone Resorption. Desferal (100 μM), a chelator of iron and other metal ions, had no significant effect on Bone Resorption, indicating (along with the results with NAG) that ROI-scavenging rather than metal chelation is responsible for inhibition of osteoclastic Bone Resorption by PDTC. Taken together these results indicate that ROI produced by osteoclasts in the Bone slice assay are not involved in the process of Bone Resorption, but are important during osteoclast activation for Bone Resorption, possibly being involved in activation of the transcription factor NF-κB.

  • Taxol inhibits osteoclastic Bone Resorption
    Calcified Tissue International, 1995
    Co-Authors: T.j. Hall, H. Jeker, M. Schaueblin

    Abstract:

    We have examined the effect of the anti-tumor compound taxol, on osteoclastic Bone Resorption. In the Bone slice assay, taxol (0.1-0.001 microM) dose-dependently inhibited Bone Resorption with an IC50 of 0.08 microM. Osteoclast survival on Bone slices was unaffected by 0.01-1 microM taxol, but 10 microM was cytotoxic. Taxol (1 microM) also inhibited osteoclast spreading (45%) on fibronectin-coated slides. The antiproliferative effects of taxol are due to its unique ability to stabilize microtubules. Primary osteoclasts are nonproliferating end cells, so taxol probably inhibits Bone Resorption by interfering with other microtubule-dependent functions such as cell polarization, motility or vesicle exocytosis. Since these inhibitory effects on osteoclasts in vitro are seen with therapeutically relevant concentrations, taxol therapy may have beneficial side-effects e.g. inhibition of hypercalcemia and Bone metastases.

H. Jeker – 3rd expert on this subject based on the ideXlab platform

  • TAXOL INHIBITS OSTEOCLASTIC Bone Resorption
    Calcified Tissue International, 1995
    Co-Authors: T.j. Hall, H. Jeker, M. Schaueblin

    Abstract:

    We have examined the effect of the anti-tumor compound taxol, on osteoclastic Bone Resorption. In the Bone slice assay, taxol (0.1–0.001 μM) dose-dependently inhibited Bone Resorption with an IC50 of 0.08 μM. Osteoclast survival on Bone slices was unaffected by 0.01–1 μM taxol, but 10 μ M was cytotoxic. Taxol (1 μM) also ihibited osteoclast spreading (45%) on fibronectin-coated slides. The antiproliterative effects of taxol are due to its unique ability to stabilize microtubules. Primary osteoclasts are nonproliferating end cells, so taxol probably inhibits Bone Resorption by intertering with other microtubule-dependent functions such as cell polarization, motility or vesicle exocytosis. Since these inhibitory effects on osteoclasts in vitro are seen with therapeutically relevant concentrations, taxol therapy may have beneficial side-effects e.g. inhibition of hyperealcemia and Bone metastases.

  • The role of reactive oxygen intermediates in osteoclastic Bone Resorption.
    Biochemical and Biophysical Research Communications, 1995
    Co-Authors: T.j. Hall, H. Jeker, M. Schaeublin, K. Fuller, T J Chambers

    Abstract:

    Abstract Osteoclasts have been shown to produce reactive oxygen intermediates (ROI) and it has been suggested that ROI are involved in the process of Bone Resorption. ROI have also been shown to play a central role in the activation of the multisubunit transcription factor NF-κB that enhances the transcription of genes encoding defence and signaling proteins. Therefore, we have assessed the effect of pyrrolidine dithiocarbamate (PDTC), an oxygen-radical scavenger and metal chelator that is a selective and potent inhibitor of NF-κB activation, on osteoclastic Bone Resorption in the Bone slice assay. PDTC (0.001 – 0.1 mM) dose-dependently and non-cytotoxically inhibited osteoclast activity with an IC 50 of 0.01 mM. PDTC (0.01 mM) caused no change in the ratio of Resorption pit area to Resorption pit depth as measured by Lasertec confocal microscopy, indicating that ROI are not involved in the resorptive process per se . This view is supported by time-course studies showing that addition of PDTC or N-acetyl cysteine (NAG; an ROI scavenger, but not metal chelator), 6 hr after the start of the assay had no significant effect on subsequent Bone Resorption. Desferal (100 μM), a chelator of iron and other metal ions, had no significant effect on Bone Resorption, indicating (along with the results with NAG) that ROI-scavenging rather than metal chelation is responsible for inhibition of osteoclastic Bone Resorption by PDTC. Taken together these results indicate that ROI produced by osteoclasts in the Bone slice assay are not involved in the process of Bone Resorption, but are important during osteoclast activation for Bone Resorption, possibly being involved in activation of the transcription factor NF-κB.

  • Taxol inhibits osteoclastic Bone Resorption
    Calcified Tissue International, 1995
    Co-Authors: T.j. Hall, H. Jeker, M. Schaueblin

    Abstract:

    We have examined the effect of the anti-tumor compound taxol, on osteoclastic Bone Resorption. In the Bone slice assay, taxol (0.1-0.001 microM) dose-dependently inhibited Bone Resorption with an IC50 of 0.08 microM. Osteoclast survival on Bone slices was unaffected by 0.01-1 microM taxol, but 10 microM was cytotoxic. Taxol (1 microM) also inhibited osteoclast spreading (45%) on fibronectin-coated slides. The antiproliferative effects of taxol are due to its unique ability to stabilize microtubules. Primary osteoclasts are nonproliferating end cells, so taxol probably inhibits Bone Resorption by interfering with other microtubule-dependent functions such as cell polarization, motility or vesicle exocytosis. Since these inhibitory effects on osteoclasts in vitro are seen with therapeutically relevant concentrations, taxol therapy may have beneficial side-effects e.g. inhibition of hypercalcemia and Bone metastases.