Decreased osteoclastogenesis in serotonin-deficient mice
Peripheral serotonin, synthesized by tryptophan hydroxylase-1 (TPH1), has been shown to play a key role in several physiological functions. Recently, controversy has emerged about whether peripheral serotonin has any effect on bone density and remodeling.We therefore decided to investigate in detail...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2012-02, Vol.109 (7), p.2567-2572 |
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| creator | Chabbi-Achengli, Yasmine Coudert, Amélie E Callebert, Jacques Geoffroy, Valérie Côté, Francine Collet, Corinne de Vernejoul, Marie-Christine |
| description | Peripheral serotonin, synthesized by tryptophan hydroxylase-1 (TPH1), has been shown to play a key role in several physiological functions. Recently, controversy has emerged about whether peripheral serotonin has any effect on bone density and remodeling.We therefore decided to investigate in detail bone remodeling in growing and mature TPH1 knockout mice (TPH1–/–). Bone resorption in TPH1–/– mice, as assessed by biochemical markers and bone histomorphometry, was markedly decreased at both ages. Using bone marrow transplantation, we present evidence that the decrease in bone resorption in TPH1–/– mice is cell-autonomous. Cultures from TPH1–/– in the presence of macrophage colony-stimulating factor and receptor activator for NF-KB ligand (RANKL) displayed fewer osteoclasts, and the decreased differentiation could be rescued by adding serotonin. Our data also provide evidence that in the presence of RANKL, osteoclast precursors express TPH1 and synthesize serotonin. Furthermore, pharmacological inhibition of serotonin receptor 1B with SB224289, and of receptor 2A with ketanserin, also reduced the number of osteoclasts. Our findings reveal that serotonin has an important local action in bone, as it can amplify the effect of RANKL on osteoclastogenesis. |
| doi_str_mv | 10.1073/pnas.1117792109 |
| format | Article |
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Recently, controversy has emerged about whether peripheral serotonin has any effect on bone density and remodeling.We therefore decided to investigate in detail bone remodeling in growing and mature TPH1 knockout mice (TPH1–/–). Bone resorption in TPH1–/– mice, as assessed by biochemical markers and bone histomorphometry, was markedly decreased at both ages. Using bone marrow transplantation, we present evidence that the decrease in bone resorption in TPH1–/– mice is cell-autonomous. Cultures from TPH1–/– in the presence of macrophage colony-stimulating factor and receptor activator for NF-KB ligand (RANKL) displayed fewer osteoclasts, and the decreased differentiation could be rescued by adding serotonin. Our data also provide evidence that in the presence of RANKL, osteoclast precursors express TPH1 and synthesize serotonin. Furthermore, pharmacological inhibition of serotonin receptor 1B with SB224289, and of receptor 2A with ketanserin, also reduced the number of osteoclasts. Our findings reveal that serotonin has an important local action in bone, as it can amplify the effect of RANKL on osteoclastogenesis.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.1117792109</identifier><identifier>PMID: 22308416</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Age ; Allografts ; Animals ; Biochemical markers ; Biological Sciences ; biomarkers ; Bone density ; Bone histomorphometry ; Bone marrow ; bone marrow transplant ; Bone remodelling ; Bone resorption ; Bones ; Cell culture ; Cell Differentiation ; Cells ; Data processing ; ketanserin ; Life Sciences ; Macrophage colony-stimulating factor ; Mice ; Mice, Knockout ; NF- Kappa B protein ; Osteoclastogenesis ; Osteoclasts ; Osteoclasts - cytology ; Osteoprogenitor cells ; Proteins ; Rodents ; Serotonin ; Serotonin - genetics ; Serotonin receptors ; TRANCE protein ; Tryptophan ; Tryptophan Hydroxylase - genetics</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2012-02, Vol.109 (7), p.2567-2572</ispartof><rights>Copyright National Academy of Sciences Feb 14, 2012</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c632t-41603ff4b8c46bdf8c8c28ac8b8f7ad69841cde1ce560266ec6744eb845b24713</citedby><cites>FETCH-LOGICAL-c632t-41603ff4b8c46bdf8c8c28ac8b8f7ad69841cde1ce560266ec6744eb845b24713</cites><orcidid>0000-0002-6496-7566</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/109/7.cover.gif</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3289318/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3289318/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22308416$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-00739938$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Chabbi-Achengli, Yasmine</creatorcontrib><creatorcontrib>Coudert, Amélie E</creatorcontrib><creatorcontrib>Callebert, Jacques</creatorcontrib><creatorcontrib>Geoffroy, Valérie</creatorcontrib><creatorcontrib>Côté, Francine</creatorcontrib><creatorcontrib>Collet, Corinne</creatorcontrib><creatorcontrib>de Vernejoul, Marie-Christine</creatorcontrib><title>Decreased osteoclastogenesis in serotonin-deficient mice</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Peripheral serotonin, synthesized by tryptophan hydroxylase-1 (TPH1), has been shown to play a key role in several physiological functions. 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Recently, controversy has emerged about whether peripheral serotonin has any effect on bone density and remodeling.We therefore decided to investigate in detail bone remodeling in growing and mature TPH1 knockout mice (TPH1–/–). Bone resorption in TPH1–/– mice, as assessed by biochemical markers and bone histomorphometry, was markedly decreased at both ages. Using bone marrow transplantation, we present evidence that the decrease in bone resorption in TPH1–/– mice is cell-autonomous. Cultures from TPH1–/– in the presence of macrophage colony-stimulating factor and receptor activator for NF-KB ligand (RANKL) displayed fewer osteoclasts, and the decreased differentiation could be rescued by adding serotonin. Our data also provide evidence that in the presence of RANKL, osteoclast precursors express TPH1 and synthesize serotonin. Furthermore, pharmacological inhibition of serotonin receptor 1B with SB224289, and of receptor 2A with ketanserin, also reduced the number of osteoclasts. 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| source | Jstor Complete Legacy; MEDLINE; PubMed Central; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry |
| subjects | Age Allografts Animals Biochemical markers Biological Sciences biomarkers Bone density Bone histomorphometry Bone marrow bone marrow transplant Bone remodelling Bone resorption Bones Cell culture Cell Differentiation Cells Data processing ketanserin Life Sciences Macrophage colony-stimulating factor Mice Mice, Knockout NF- Kappa B protein Osteoclastogenesis Osteoclasts Osteoclasts - cytology Osteoprogenitor cells Proteins Rodents Serotonin Serotonin - genetics Serotonin receptors TRANCE protein Tryptophan Tryptophan Hydroxylase - genetics |
| title | Decreased osteoclastogenesis in serotonin-deficient mice |
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