Disruption of Jmjd3/p16 Ink4a Signaling Pathway Causes Bizarre Parosteal Osteochondromatous Proliferation (BPOP)-like Lesion in Mice
Bizarre parosteal osteochondromatous proliferation (BPOP), or Nora's lesion, is a rare benign osteochondromatous lesion. At present, the molecular etiology of BPOP remains unclear. JMJD3(KDM6B) is an H3K27me3 demethylase and counteracts polycomb-mediated transcription repression. Previously, Jm...
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| Veröffentlicht in: | Journal of bone and mineral research 2021-10, Vol.36 (10), p.1931 |
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| creator | Zhang, Feng Wang, Yingmei Wang, Yuying Wang, Xinli Zhang, Dawei Zhao, Xiong Jiang, Runmin Gu, Yu Yang, Guifang Fu, Xin Xu, Longyong Xu, Longxia Zheng, Liting Zhang, Jing Li, Zengshan Yan, Qingguo Shi, Jianguo Roessner, Albert Wang, Zhe Li, Qing Ye, Jing Chen, Charlie Degui Guo, Shuangping Min, Jie |
| description | Bizarre parosteal osteochondromatous proliferation (BPOP), or Nora's lesion, is a rare benign osteochondromatous lesion. At present, the molecular etiology of BPOP remains unclear. JMJD3(KDM6B) is an H3K27me3 demethylase and counteracts polycomb-mediated transcription repression. Previously, Jmjd3 was shown to be critical for bone development and osteoarthritis. Here, we report that conditional deletion of Jmjd3 in chondrogenic cells unexpectedly resulted in BPOP-like lesion in mice. Biochemical investigations revealed that Jmjd3 inhibited BPOP-like lesion through p16
. Immunohistochemistry and RT-qPCR assays indicated JMJD3 and p16
level were significantly reduced in human BPOP lesion compared with normal subjects. This was further confirmed by Jmjd3/Ink4a double-gene knockout mice experiments. Therefore, our results indicated the pathway of Jmjd3/p16
may be essential for the development of BPOP in human. © 2021 American Society for Bone and Mineral Research (ASBMR). |
| format | Article |
| fullrecord | <record><control><sourceid>pubmed</sourceid><recordid>TN_cdi_pubmed_primary_34173271</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>34173271</sourcerecordid><originalsourceid>FETCH-pubmed_primary_341732713</originalsourceid><addsrcrecordid>eNqFjk1Lw0AQhhdBbP34CzJHPQSz3XTruVVRURrQexmbSTvtZjfMJEg9-8OtomdPDzy8PLwHZmjHI5cV_toOzLHqJs9zP_b-yAxcYSduNLFD83nDKn3bcYqQanhsNpW7aq2Hh7gtEF54FTFwXEGJ3foddzDDXklhyh8oQnstSTvCAPM90nKdYiWpwS71CqWkwDUJ_uQvpuW8vMwCbwmeSL8VR3jmJZ2awxqD0tkvT8z53e3r7D5r-7eGqkUr3KDsFn-33b-DL5NoTkE</addsrcrecordid><sourcetype>Index Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Disruption of Jmjd3/p16 Ink4a Signaling Pathway Causes Bizarre Parosteal Osteochondromatous Proliferation (BPOP)-like Lesion in Mice</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Access via Wiley Online Library</source><source>Oxford University Press Journals All Titles (1996-Current)</source><creator>Zhang, Feng ; Wang, Yingmei ; Wang, Yuying ; Wang, Xinli ; Zhang, Dawei ; Zhao, Xiong ; Jiang, Runmin ; Gu, Yu ; Yang, Guifang ; Fu, Xin ; Xu, Longyong ; Xu, Longxia ; Zheng, Liting ; Zhang, Jing ; Li, Zengshan ; Yan, Qingguo ; Shi, Jianguo ; Roessner, Albert ; Wang, Zhe ; Li, Qing ; Ye, Jing ; Chen, Charlie Degui ; Guo, Shuangping ; Min, Jie</creator><creatorcontrib>Zhang, Feng ; Wang, Yingmei ; Wang, Yuying ; Wang, Xinli ; Zhang, Dawei ; Zhao, Xiong ; Jiang, Runmin ; Gu, Yu ; Yang, Guifang ; Fu, Xin ; Xu, Longyong ; Xu, Longxia ; Zheng, Liting ; Zhang, Jing ; Li, Zengshan ; Yan, Qingguo ; Shi, Jianguo ; Roessner, Albert ; Wang, Zhe ; Li, Qing ; Ye, Jing ; Chen, Charlie Degui ; Guo, Shuangping ; Min, Jie</creatorcontrib><description>Bizarre parosteal osteochondromatous proliferation (BPOP), or Nora's lesion, is a rare benign osteochondromatous lesion. At present, the molecular etiology of BPOP remains unclear. JMJD3(KDM6B) is an H3K27me3 demethylase and counteracts polycomb-mediated transcription repression. Previously, Jmjd3 was shown to be critical for bone development and osteoarthritis. Here, we report that conditional deletion of Jmjd3 in chondrogenic cells unexpectedly resulted in BPOP-like lesion in mice. Biochemical investigations revealed that Jmjd3 inhibited BPOP-like lesion through p16
. Immunohistochemistry and RT-qPCR assays indicated JMJD3 and p16
level were significantly reduced in human BPOP lesion compared with normal subjects. This was further confirmed by Jmjd3/Ink4a double-gene knockout mice experiments. Therefore, our results indicated the pathway of Jmjd3/p16
may be essential for the development of BPOP in human. © 2021 American Society for Bone and Mineral Research (ASBMR).</description><identifier>EISSN: 1523-4681</identifier><identifier>PMID: 34173271</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Bone Neoplasms ; Cell Proliferation ; Cyclin-Dependent Kinase Inhibitor p16 - genetics ; Mice ; Osteochondroma - genetics ; Signal Transduction</subject><ispartof>Journal of bone and mineral research, 2021-10, Vol.36 (10), p.1931</ispartof><rights>2021 American Society for Bone and Mineral Research (ASBMR).</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0000-0003-2034-5324</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34173271$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Feng</creatorcontrib><creatorcontrib>Wang, Yingmei</creatorcontrib><creatorcontrib>Wang, Yuying</creatorcontrib><creatorcontrib>Wang, Xinli</creatorcontrib><creatorcontrib>Zhang, Dawei</creatorcontrib><creatorcontrib>Zhao, Xiong</creatorcontrib><creatorcontrib>Jiang, Runmin</creatorcontrib><creatorcontrib>Gu, Yu</creatorcontrib><creatorcontrib>Yang, Guifang</creatorcontrib><creatorcontrib>Fu, Xin</creatorcontrib><creatorcontrib>Xu, Longyong</creatorcontrib><creatorcontrib>Xu, Longxia</creatorcontrib><creatorcontrib>Zheng, Liting</creatorcontrib><creatorcontrib>Zhang, Jing</creatorcontrib><creatorcontrib>Li, Zengshan</creatorcontrib><creatorcontrib>Yan, Qingguo</creatorcontrib><creatorcontrib>Shi, Jianguo</creatorcontrib><creatorcontrib>Roessner, Albert</creatorcontrib><creatorcontrib>Wang, Zhe</creatorcontrib><creatorcontrib>Li, Qing</creatorcontrib><creatorcontrib>Ye, Jing</creatorcontrib><creatorcontrib>Chen, Charlie Degui</creatorcontrib><creatorcontrib>Guo, Shuangping</creatorcontrib><creatorcontrib>Min, Jie</creatorcontrib><title>Disruption of Jmjd3/p16 Ink4a Signaling Pathway Causes Bizarre Parosteal Osteochondromatous Proliferation (BPOP)-like Lesion in Mice</title><title>Journal of bone and mineral research</title><addtitle>J Bone Miner Res</addtitle><description>Bizarre parosteal osteochondromatous proliferation (BPOP), or Nora's lesion, is a rare benign osteochondromatous lesion. At present, the molecular etiology of BPOP remains unclear. JMJD3(KDM6B) is an H3K27me3 demethylase and counteracts polycomb-mediated transcription repression. Previously, Jmjd3 was shown to be critical for bone development and osteoarthritis. Here, we report that conditional deletion of Jmjd3 in chondrogenic cells unexpectedly resulted in BPOP-like lesion in mice. Biochemical investigations revealed that Jmjd3 inhibited BPOP-like lesion through p16
. Immunohistochemistry and RT-qPCR assays indicated JMJD3 and p16
level were significantly reduced in human BPOP lesion compared with normal subjects. This was further confirmed by Jmjd3/Ink4a double-gene knockout mice experiments. Therefore, our results indicated the pathway of Jmjd3/p16
may be essential for the development of BPOP in human. © 2021 American Society for Bone and Mineral Research (ASBMR).</description><subject>Animals</subject><subject>Bone Neoplasms</subject><subject>Cell Proliferation</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - genetics</subject><subject>Mice</subject><subject>Osteochondroma - genetics</subject><subject>Signal Transduction</subject><issn>1523-4681</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFjk1Lw0AQhhdBbP34CzJHPQSz3XTruVVRURrQexmbSTvtZjfMJEg9-8OtomdPDzy8PLwHZmjHI5cV_toOzLHqJs9zP_b-yAxcYSduNLFD83nDKn3bcYqQanhsNpW7aq2Hh7gtEF54FTFwXEGJ3foddzDDXklhyh8oQnstSTvCAPM90nKdYiWpwS71CqWkwDUJ_uQvpuW8vMwCbwmeSL8VR3jmJZ2awxqD0tkvT8z53e3r7D5r-7eGqkUr3KDsFn-33b-DL5NoTkE</recordid><startdate>202110</startdate><enddate>202110</enddate><creator>Zhang, Feng</creator><creator>Wang, Yingmei</creator><creator>Wang, Yuying</creator><creator>Wang, Xinli</creator><creator>Zhang, Dawei</creator><creator>Zhao, Xiong</creator><creator>Jiang, Runmin</creator><creator>Gu, Yu</creator><creator>Yang, Guifang</creator><creator>Fu, Xin</creator><creator>Xu, Longyong</creator><creator>Xu, Longxia</creator><creator>Zheng, Liting</creator><creator>Zhang, Jing</creator><creator>Li, Zengshan</creator><creator>Yan, Qingguo</creator><creator>Shi, Jianguo</creator><creator>Roessner, Albert</creator><creator>Wang, Zhe</creator><creator>Li, Qing</creator><creator>Ye, Jing</creator><creator>Chen, Charlie Degui</creator><creator>Guo, Shuangping</creator><creator>Min, Jie</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><orcidid>https://orcid.org/0000-0003-2034-5324</orcidid></search><sort><creationdate>202110</creationdate><title>Disruption of Jmjd3/p16 Ink4a Signaling Pathway Causes Bizarre Parosteal Osteochondromatous Proliferation (BPOP)-like Lesion in Mice</title><author>Zhang, Feng ; Wang, Yingmei ; Wang, Yuying ; Wang, Xinli ; Zhang, Dawei ; Zhao, Xiong ; Jiang, Runmin ; Gu, Yu ; Yang, Guifang ; Fu, Xin ; Xu, Longyong ; Xu, Longxia ; Zheng, Liting ; Zhang, Jing ; Li, Zengshan ; Yan, Qingguo ; Shi, Jianguo ; Roessner, Albert ; Wang, Zhe ; Li, Qing ; Ye, Jing ; Chen, Charlie Degui ; Guo, Shuangping ; Min, Jie</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-pubmed_primary_341732713</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Bone Neoplasms</topic><topic>Cell Proliferation</topic><topic>Cyclin-Dependent Kinase Inhibitor p16 - genetics</topic><topic>Mice</topic><topic>Osteochondroma - genetics</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Feng</creatorcontrib><creatorcontrib>Wang, Yingmei</creatorcontrib><creatorcontrib>Wang, Yuying</creatorcontrib><creatorcontrib>Wang, Xinli</creatorcontrib><creatorcontrib>Zhang, Dawei</creatorcontrib><creatorcontrib>Zhao, Xiong</creatorcontrib><creatorcontrib>Jiang, Runmin</creatorcontrib><creatorcontrib>Gu, Yu</creatorcontrib><creatorcontrib>Yang, Guifang</creatorcontrib><creatorcontrib>Fu, Xin</creatorcontrib><creatorcontrib>Xu, Longyong</creatorcontrib><creatorcontrib>Xu, Longxia</creatorcontrib><creatorcontrib>Zheng, Liting</creatorcontrib><creatorcontrib>Zhang, Jing</creatorcontrib><creatorcontrib>Li, Zengshan</creatorcontrib><creatorcontrib>Yan, Qingguo</creatorcontrib><creatorcontrib>Shi, Jianguo</creatorcontrib><creatorcontrib>Roessner, Albert</creatorcontrib><creatorcontrib>Wang, Zhe</creatorcontrib><creatorcontrib>Li, Qing</creatorcontrib><creatorcontrib>Ye, Jing</creatorcontrib><creatorcontrib>Chen, Charlie Degui</creatorcontrib><creatorcontrib>Guo, Shuangping</creatorcontrib><creatorcontrib>Min, Jie</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Journal of bone and mineral research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Feng</au><au>Wang, Yingmei</au><au>Wang, Yuying</au><au>Wang, Xinli</au><au>Zhang, Dawei</au><au>Zhao, Xiong</au><au>Jiang, Runmin</au><au>Gu, Yu</au><au>Yang, Guifang</au><au>Fu, Xin</au><au>Xu, Longyong</au><au>Xu, Longxia</au><au>Zheng, Liting</au><au>Zhang, Jing</au><au>Li, Zengshan</au><au>Yan, Qingguo</au><au>Shi, Jianguo</au><au>Roessner, Albert</au><au>Wang, Zhe</au><au>Li, Qing</au><au>Ye, Jing</au><au>Chen, Charlie Degui</au><au>Guo, Shuangping</au><au>Min, Jie</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Disruption of Jmjd3/p16 Ink4a Signaling Pathway Causes Bizarre Parosteal Osteochondromatous Proliferation (BPOP)-like Lesion in Mice</atitle><jtitle>Journal of bone and mineral research</jtitle><addtitle>J Bone Miner Res</addtitle><date>2021-10</date><risdate>2021</risdate><volume>36</volume><issue>10</issue><spage>1931</spage><pages>1931-</pages><eissn>1523-4681</eissn><abstract>Bizarre parosteal osteochondromatous proliferation (BPOP), or Nora's lesion, is a rare benign osteochondromatous lesion. At present, the molecular etiology of BPOP remains unclear. JMJD3(KDM6B) is an H3K27me3 demethylase and counteracts polycomb-mediated transcription repression. Previously, Jmjd3 was shown to be critical for bone development and osteoarthritis. Here, we report that conditional deletion of Jmjd3 in chondrogenic cells unexpectedly resulted in BPOP-like lesion in mice. Biochemical investigations revealed that Jmjd3 inhibited BPOP-like lesion through p16
. Immunohistochemistry and RT-qPCR assays indicated JMJD3 and p16
level were significantly reduced in human BPOP lesion compared with normal subjects. This was further confirmed by Jmjd3/Ink4a double-gene knockout mice experiments. Therefore, our results indicated the pathway of Jmjd3/p16
may be essential for the development of BPOP in human. © 2021 American Society for Bone and Mineral Research (ASBMR).</abstract><cop>United States</cop><pmid>34173271</pmid><orcidid>https://orcid.org/0000-0003-2034-5324</orcidid></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Access via Wiley Online Library; Oxford University Press Journals All Titles (1996-Current) |
| subjects | Animals Bone Neoplasms Cell Proliferation Cyclin-Dependent Kinase Inhibitor p16 - genetics Mice Osteochondroma - genetics Signal Transduction |
| title | Disruption of Jmjd3/p16 Ink4a Signaling Pathway Causes Bizarre Parosteal Osteochondromatous Proliferation (BPOP)-like Lesion in Mice |
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