Hepatocyte growth factor can substitute for M-CSF to support osteoclastogenesis.
Osteopetrotic mice lacking functional macrophage-colony stimulating factor (M-CSF) recover with ageing, suggesting that alternative osteoclastogenesis pathways exist. Hepatocyte growth factor (HGF) and M-CSF signal through tyrosine kinase receptors and phosphorylate common transducers and effectors...
| Main Authors: | , , , |
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| Format: | Journal article |
| Language: | English |
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2006
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| _version_ | 1797087962911997952 |
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| author | Adamopoulos, I Xia, Z Lau, Y Athanasou, N |
| author_facet | Adamopoulos, I Xia, Z Lau, Y Athanasou, N |
| author_sort | Adamopoulos, I |
| collection | OXFORD |
| description | Osteopetrotic mice lacking functional macrophage-colony stimulating factor (M-CSF) recover with ageing, suggesting that alternative osteoclastogenesis pathways exist. Hepatocyte growth factor (HGF) and M-CSF signal through tyrosine kinase receptors and phosphorylate common transducers and effectors such as Src, Grb2, and PI3-Kinase. HGF is known to play a role in osteoclast formation, and in this study we have determined whether HGF could replace M-CSF to support human osteoclastogenesis. We found that the HGF receptor, c-Met, is expressed by the CD14(+) monocyte fraction of human peripheral blood mononuclear cells (PBMC). HGF was able to support monocyte-osteoclast differentiation in the presence of receptor activator for nuclear factor kappaB ligand as evidenced by the formation of numerous multinucleated tartrate-resistant acid phosphatase and vitronectin receptor positive cells which formed F-actin rings and were capable of lacunar resorption. The addition of a neutralising antibody to M-CSF did not inhibit osteoclast differentiation. HGF is a well-established survival factor and viability assays and live/dead staining showed that it promoted the survival and proliferation of monocytes and osteoclasts in a manner similar to M-CSF. Our findings indicate that HGF can substitute for M-CSF to support human osteoclast formation. |
| first_indexed | 2024-03-07T02:43:04Z |
| format | Journal article |
| id | oxford-uuid:ab1e5773-241b-4c06-a38d-834e537fe6ab |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-07T02:43:04Z |
| publishDate | 2006 |
| record_format | dspace |
| spelling | oxford-uuid:ab1e5773-241b-4c06-a38d-834e537fe6ab2022-03-27T03:19:41ZHepatocyte growth factor can substitute for M-CSF to support osteoclastogenesis.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:ab1e5773-241b-4c06-a38d-834e537fe6abEnglishSymplectic Elements at Oxford2006Adamopoulos, IXia, ZLau, YAthanasou, NOsteopetrotic mice lacking functional macrophage-colony stimulating factor (M-CSF) recover with ageing, suggesting that alternative osteoclastogenesis pathways exist. Hepatocyte growth factor (HGF) and M-CSF signal through tyrosine kinase receptors and phosphorylate common transducers and effectors such as Src, Grb2, and PI3-Kinase. HGF is known to play a role in osteoclast formation, and in this study we have determined whether HGF could replace M-CSF to support human osteoclastogenesis. We found that the HGF receptor, c-Met, is expressed by the CD14(+) monocyte fraction of human peripheral blood mononuclear cells (PBMC). HGF was able to support monocyte-osteoclast differentiation in the presence of receptor activator for nuclear factor kappaB ligand as evidenced by the formation of numerous multinucleated tartrate-resistant acid phosphatase and vitronectin receptor positive cells which formed F-actin rings and were capable of lacunar resorption. The addition of a neutralising antibody to M-CSF did not inhibit osteoclast differentiation. HGF is a well-established survival factor and viability assays and live/dead staining showed that it promoted the survival and proliferation of monocytes and osteoclasts in a manner similar to M-CSF. Our findings indicate that HGF can substitute for M-CSF to support human osteoclast formation. |
| spellingShingle | Adamopoulos, I Xia, Z Lau, Y Athanasou, N Hepatocyte growth factor can substitute for M-CSF to support osteoclastogenesis. |
| title | Hepatocyte growth factor can substitute for M-CSF to support osteoclastogenesis. |
| title_full | Hepatocyte growth factor can substitute for M-CSF to support osteoclastogenesis. |
| title_fullStr | Hepatocyte growth factor can substitute for M-CSF to support osteoclastogenesis. |
| title_full_unstemmed | Hepatocyte growth factor can substitute for M-CSF to support osteoclastogenesis. |
| title_short | Hepatocyte growth factor can substitute for M-CSF to support osteoclastogenesis. |
| title_sort | hepatocyte growth factor can substitute for m csf to support osteoclastogenesis |
| work_keys_str_mv | AT adamopoulosi hepatocytegrowthfactorcansubstituteformcsftosupportosteoclastogenesis AT xiaz hepatocytegrowthfactorcansubstituteformcsftosupportosteoclastogenesis AT lauy hepatocytegrowthfactorcansubstituteformcsftosupportosteoclastogenesis AT athanasoun hepatocytegrowthfactorcansubstituteformcsftosupportosteoclastogenesis |