Wnt-mediated reciprocal regulation between cartilage and bone development during endochondral ossification
Abstract The role of Wnt signaling is extensively studied in skeletal development and postnatal bone remodeling, mostly based on the genetic approaches of β-catenin manipulation. However, given their independent function, a requirement for β-catenin is not the same as that for Wnt. Here, we investig...
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Veröffentlicht in: | Bone (New York, N.Y.) N.Y.), 2013-04, Vol.53 (2), p.566-574 |
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creator | Lu, Cheng Wan, Yong Cao, Jingjing Zhu, Xuming Yu, Jian Zhou, Rujiang Yao, Yiyun Zhang, Lingling Zhao, Haixia Li, Hanjun Zhao, Jianzhi He, Lin Ma, Gang Yang, Xiao Yao, Zhengju Guo, Xizhi |
description | Abstract The role of Wnt signaling is extensively studied in skeletal development and postnatal bone remodeling, mostly based on the genetic approaches of β-catenin manipulation. However, given their independent function, a requirement for β-catenin is not the same as that for Wnt. Here, we investigated the effect of Wnt proteins in both tissues through generating cartilage- or bone-specific Wls null mice, respectively. Depletion of Wls by Col2-Cre , which would block Wnt secretion in the chondrocytes and perichondrium, delayed chondrocyte hypertrophy in the growth plate and impaired perichondrial osteogenesis. Loss of Wls in chondrocytes also disturbed the proliferating chondrocyte morphology and division orientation, which was similar to the defect observed in Wnt5a null mice. On the other hand, inactivation of Wls in osteoblasts by Col1-Cre resulted in a shorter hypertrophic zone and an increase of TRAP positive cell number in the chondro-osseous junction of growth plate, coupled with a decrease in bone mass. Taken together, our studies reveal that Wnt proteins not only modulate differentiation and cellular communication within populations of chondrocytes, but also mediate the cross regulation between the chondrocytes and osteoblasts in growth plate. |
doi_str_mv | 10.1016/j.bone.2012.12.016 |
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However, given their independent function, a requirement for β-catenin is not the same as that for Wnt. Here, we investigated the effect of Wnt proteins in both tissues through generating cartilage- or bone-specific Wls null mice, respectively. Depletion of Wls by Col2-Cre , which would block Wnt secretion in the chondrocytes and perichondrium, delayed chondrocyte hypertrophy in the growth plate and impaired perichondrial osteogenesis. Loss of Wls in chondrocytes also disturbed the proliferating chondrocyte morphology and division orientation, which was similar to the defect observed in Wnt5a null mice. On the other hand, inactivation of Wls in osteoblasts by Col1-Cre resulted in a shorter hypertrophic zone and an increase of TRAP positive cell number in the chondro-osseous junction of growth plate, coupled with a decrease in bone mass. Taken together, our studies reveal that Wnt proteins not only modulate differentiation and cellular communication within populations of chondrocytes, but also mediate the cross regulation between the chondrocytes and osteoblasts in growth plate.</description><identifier>ISSN: 8756-3282</identifier><identifier>EISSN: 1873-2763</identifier><identifier>DOI: 10.1016/j.bone.2012.12.016</identifier><identifier>PMID: 23274346</identifier><language>eng</language><publisher>Amsterdam: Elsevier Inc</publisher><subject>Animals ; Biological and medical sciences ; Bone ; Bone Development - genetics ; Bone Development - physiology ; Cartilage ; Cartilage - growth & development ; Cartilage - metabolism ; Division orientation ; Female ; Fundamental and applied biological sciences. Psychology ; Immunohistochemistry ; In Situ Hybridization ; Intracellular Signaling Peptides and Proteins - genetics ; Intracellular Signaling Peptides and Proteins - metabolism ; Male ; Mice ; Orthopedics ; Perichondrial ossification ; Receptors, G-Protein-Coupled ; Vertebrates: anatomy and physiology, studies on body, several organs or systems ; Wls ; Wnt Proteins - genetics ; Wnt Proteins - metabolism</subject><ispartof>Bone (New York, N.Y.), 2013-04, Vol.53 (2), p.566-574</ispartof><rights>Elsevier Inc.</rights><rights>2012 Elsevier Inc.</rights><rights>2014 INIST-CNRS</rights><rights>Copyright © 2012 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c511t-238bbd4659bfaa3c91d29e903042b752073c4dfaf75d0dfb7444338a03b0501c3</citedby><cites>FETCH-LOGICAL-c511t-238bbd4659bfaa3c91d29e903042b752073c4dfaf75d0dfb7444338a03b0501c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S8756328212014342$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27903,27904,65309</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27286257$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23274346$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lu, Cheng</creatorcontrib><creatorcontrib>Wan, Yong</creatorcontrib><creatorcontrib>Cao, Jingjing</creatorcontrib><creatorcontrib>Zhu, Xuming</creatorcontrib><creatorcontrib>Yu, Jian</creatorcontrib><creatorcontrib>Zhou, Rujiang</creatorcontrib><creatorcontrib>Yao, Yiyun</creatorcontrib><creatorcontrib>Zhang, Lingling</creatorcontrib><creatorcontrib>Zhao, Haixia</creatorcontrib><creatorcontrib>Li, Hanjun</creatorcontrib><creatorcontrib>Zhao, Jianzhi</creatorcontrib><creatorcontrib>He, Lin</creatorcontrib><creatorcontrib>Ma, Gang</creatorcontrib><creatorcontrib>Yang, Xiao</creatorcontrib><creatorcontrib>Yao, Zhengju</creatorcontrib><creatorcontrib>Guo, Xizhi</creatorcontrib><title>Wnt-mediated reciprocal regulation between cartilage and bone development during endochondral ossification</title><title>Bone (New York, N.Y.)</title><addtitle>Bone</addtitle><description>Abstract The role of Wnt signaling is extensively studied in skeletal development and postnatal bone remodeling, mostly based on the genetic approaches of β-catenin manipulation. However, given their independent function, a requirement for β-catenin is not the same as that for Wnt. Here, we investigated the effect of Wnt proteins in both tissues through generating cartilage- or bone-specific Wls null mice, respectively. Depletion of Wls by Col2-Cre , which would block Wnt secretion in the chondrocytes and perichondrium, delayed chondrocyte hypertrophy in the growth plate and impaired perichondrial osteogenesis. Loss of Wls in chondrocytes also disturbed the proliferating chondrocyte morphology and division orientation, which was similar to the defect observed in Wnt5a null mice. On the other hand, inactivation of Wls in osteoblasts by Col1-Cre resulted in a shorter hypertrophic zone and an increase of TRAP positive cell number in the chondro-osseous junction of growth plate, coupled with a decrease in bone mass. Taken together, our studies reveal that Wnt proteins not only modulate differentiation and cellular communication within populations of chondrocytes, but also mediate the cross regulation between the chondrocytes and osteoblasts in growth plate.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bone</subject><subject>Bone Development - genetics</subject><subject>Bone Development - physiology</subject><subject>Cartilage</subject><subject>Cartilage - growth & development</subject><subject>Cartilage - metabolism</subject><subject>Division orientation</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Immunohistochemistry</subject><subject>In Situ Hybridization</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Orthopedics</subject><subject>Perichondrial ossification</subject><subject>Receptors, G-Protein-Coupled</subject><subject>Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><subject>Wls</subject><subject>Wnt Proteins - genetics</subject><subject>Wnt Proteins - metabolism</subject><issn>8756-3282</issn><issn>1873-2763</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kk2LFDEQhoMo7rj6BzxIXwQvPearO90ggix-wcIeVvEY0kn1mDaTjEn3LvvvrXZGhT0IBQnFW2-qnhQhzxndMsra19N2SBG2nDK-xcDUA7JhnRI1V614SDadatpa8I6fkSelTJRS0Sv2mJxxwZUUst2Q6Vuc6z04b2ZwVQbrDzlZE_C6W4KZfYrVAPMtQKysybMPZgeVia5a364c3EBIhz3EuXJL9nFXQXTJfk_RZXRJpfjR298-T8mj0YQCz07nOfn64f2Xi0_15dXHzxfvLmvbMDbXXHTD4GTb9MNojLA9c7yHngoq-aAaTpWw0o1mVI2jbhyUlFKIzlAx0IYyK87Jq6MvTvJzgTLrvS8WQjAR0lI0E0wq2vRtj1J-lNqMnWYY9SH7vcl3mlG9MtaTXufUK2ONgSksenHyXwYk97fkD1QUvDwJTEGUYzbR-vJPp3jX8kah7s1RB0jjxkPWxXqIFn8DP2LWLvn_9_H2XrkNPiLs8APuoExpyRE5a6YLFujrdRvWZWBogn1y8QsIZbCt</recordid><startdate>20130401</startdate><enddate>20130401</enddate><creator>Lu, Cheng</creator><creator>Wan, Yong</creator><creator>Cao, Jingjing</creator><creator>Zhu, Xuming</creator><creator>Yu, Jian</creator><creator>Zhou, Rujiang</creator><creator>Yao, Yiyun</creator><creator>Zhang, Lingling</creator><creator>Zhao, Haixia</creator><creator>Li, Hanjun</creator><creator>Zhao, Jianzhi</creator><creator>He, Lin</creator><creator>Ma, Gang</creator><creator>Yang, Xiao</creator><creator>Yao, Zhengju</creator><creator>Guo, Xizhi</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20130401</creationdate><title>Wnt-mediated reciprocal regulation between cartilage and bone development during endochondral ossification</title><author>Lu, Cheng ; Wan, Yong ; Cao, Jingjing ; Zhu, Xuming ; Yu, Jian ; Zhou, Rujiang ; Yao, Yiyun ; Zhang, Lingling ; Zhao, Haixia ; Li, Hanjun ; Zhao, Jianzhi ; He, Lin ; Ma, Gang ; Yang, Xiao ; Yao, Zhengju ; Guo, Xizhi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c511t-238bbd4659bfaa3c91d29e903042b752073c4dfaf75d0dfb7444338a03b0501c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bone</topic><topic>Bone Development - genetics</topic><topic>Bone Development - physiology</topic><topic>Cartilage</topic><topic>Cartilage - growth & development</topic><topic>Cartilage - metabolism</topic><topic>Division orientation</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. 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However, given their independent function, a requirement for β-catenin is not the same as that for Wnt. Here, we investigated the effect of Wnt proteins in both tissues through generating cartilage- or bone-specific Wls null mice, respectively. Depletion of Wls by Col2-Cre , which would block Wnt secretion in the chondrocytes and perichondrium, delayed chondrocyte hypertrophy in the growth plate and impaired perichondrial osteogenesis. Loss of Wls in chondrocytes also disturbed the proliferating chondrocyte morphology and division orientation, which was similar to the defect observed in Wnt5a null mice. On the other hand, inactivation of Wls in osteoblasts by Col1-Cre resulted in a shorter hypertrophic zone and an increase of TRAP positive cell number in the chondro-osseous junction of growth plate, coupled with a decrease in bone mass. Taken together, our studies reveal that Wnt proteins not only modulate differentiation and cellular communication within populations of chondrocytes, but also mediate the cross regulation between the chondrocytes and osteoblasts in growth plate.</abstract><cop>Amsterdam</cop><pub>Elsevier Inc</pub><pmid>23274346</pmid><doi>10.1016/j.bone.2012.12.016</doi><tpages>9</tpages></addata></record> |
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subjects | Animals Biological and medical sciences Bone Bone Development - genetics Bone Development - physiology Cartilage Cartilage - growth & development Cartilage - metabolism Division orientation Female Fundamental and applied biological sciences. Psychology Immunohistochemistry In Situ Hybridization Intracellular Signaling Peptides and Proteins - genetics Intracellular Signaling Peptides and Proteins - metabolism Male Mice Orthopedics Perichondrial ossification Receptors, G-Protein-Coupled Vertebrates: anatomy and physiology, studies on body, several organs or systems Wls Wnt Proteins - genetics Wnt Proteins - metabolism |
title | Wnt-mediated reciprocal regulation between cartilage and bone development during endochondral ossification |
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