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Endostatin inhibits VEGF-A induced osteoclastic bone resorption in vitro

BACKGROUND: Endostatin is a C-terminal fragment of collagen XVIII which is a component of basement membranes with the structural properties of both collagens and proteoglycans. Endostatin has a major role in angiogenesis which is intimately associated with bone development and remodeling. Signaling...

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Autores principales: Sipola, Annina, Nelo, Katri, Hautala, Timo, Ilvesaro, Joanna, Tuukkanen, Juha
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2006
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1534045/
https://www.ncbi.nlm.nih.gov/pubmed/16839420
http://dx.doi.org/10.1186/1471-2474-7-56
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author Sipola, Annina
Nelo, Katri
Hautala, Timo
Ilvesaro, Joanna
Tuukkanen, Juha
author_facet Sipola, Annina
Nelo, Katri
Hautala, Timo
Ilvesaro, Joanna
Tuukkanen, Juha
author_sort Sipola, Annina
collection PubMed
description BACKGROUND: Endostatin is a C-terminal fragment of collagen XVIII which is a component of basement membranes with the structural properties of both collagens and proteoglycans. Endostatin has a major role in angiogenesis which is intimately associated with bone development and remodeling. Signaling between the endothelial cells and the bone cells, for example, may have a role in recruitment of osteoclastic precursor cells. Our study aims at exploring a possibility that endostatin, either as a part of basement membrane or as a soluble molecule, may control osteoclastogenesis and osteoclastic bone resorption in vitro. METHODS: Rat pit formation assay was employed in order to examine the effect of endostatin alone or in combination with vascular endothelial growth factor-A (VEGF-A) on bone resorption in vitro. Effect of these agents on osteoclast differentiation in vitro was also tested. Osteoclastogenesis and the number of osteoclasts were followed by tartrate resistant acid phosphatase (TRACP) staining and resorption was evaluated by measuring the area of excavated pits. RESULTS: Endostatin inhibited the VEGF-A stimulated osteoclastic bone resorption, whereas endostatin alone had no effect on the basal resorption level in the absence of VEGF-A. In addition, endostatin could inhibit osteoclast differentiation in vitro independent of VEGF-A. CONCLUSION: Our in vitro data indicate that collagen XVIII/endostatin can suppress VEGF-A induced osteoclastic bone resorption to the basal level. Osteoclastogenesis is also inhibited by endostatin. The regulatory effect of endostatin, however, is not critical since endostatin alone does not modify the basal bone resorption.
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spelling pubmed-15340452006-08-09 Endostatin inhibits VEGF-A induced osteoclastic bone resorption in vitro Sipola, Annina Nelo, Katri Hautala, Timo Ilvesaro, Joanna Tuukkanen, Juha BMC Musculoskelet Disord Research Article BACKGROUND: Endostatin is a C-terminal fragment of collagen XVIII which is a component of basement membranes with the structural properties of both collagens and proteoglycans. Endostatin has a major role in angiogenesis which is intimately associated with bone development and remodeling. Signaling between the endothelial cells and the bone cells, for example, may have a role in recruitment of osteoclastic precursor cells. Our study aims at exploring a possibility that endostatin, either as a part of basement membrane or as a soluble molecule, may control osteoclastogenesis and osteoclastic bone resorption in vitro. METHODS: Rat pit formation assay was employed in order to examine the effect of endostatin alone or in combination with vascular endothelial growth factor-A (VEGF-A) on bone resorption in vitro. Effect of these agents on osteoclast differentiation in vitro was also tested. Osteoclastogenesis and the number of osteoclasts were followed by tartrate resistant acid phosphatase (TRACP) staining and resorption was evaluated by measuring the area of excavated pits. RESULTS: Endostatin inhibited the VEGF-A stimulated osteoclastic bone resorption, whereas endostatin alone had no effect on the basal resorption level in the absence of VEGF-A. In addition, endostatin could inhibit osteoclast differentiation in vitro independent of VEGF-A. CONCLUSION: Our in vitro data indicate that collagen XVIII/endostatin can suppress VEGF-A induced osteoclastic bone resorption to the basal level. Osteoclastogenesis is also inhibited by endostatin. The regulatory effect of endostatin, however, is not critical since endostatin alone does not modify the basal bone resorption. BioMed Central 2006-07-13 /pmc/articles/PMC1534045/ /pubmed/16839420 http://dx.doi.org/10.1186/1471-2474-7-56 Text en Copyright © 2006 Sipola et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Sipola, Annina
Nelo, Katri
Hautala, Timo
Ilvesaro, Joanna
Tuukkanen, Juha
Endostatin inhibits VEGF-A induced osteoclastic bone resorption in vitro
title Endostatin inhibits VEGF-A induced osteoclastic bone resorption in vitro
title_full Endostatin inhibits VEGF-A induced osteoclastic bone resorption in vitro
title_fullStr Endostatin inhibits VEGF-A induced osteoclastic bone resorption in vitro
title_full_unstemmed Endostatin inhibits VEGF-A induced osteoclastic bone resorption in vitro
title_short Endostatin inhibits VEGF-A induced osteoclastic bone resorption in vitro
title_sort endostatin inhibits vegf-a induced osteoclastic bone resorption in vitro
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1534045/
https://www.ncbi.nlm.nih.gov/pubmed/16839420
http://dx.doi.org/10.1186/1471-2474-7-56
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