Targeted overexpression of the long noncoding RNA ODSM can regulate osteoblast function in vitro and in vivo
Ameliorating bone loss caused by mechanical unloading is a substantial clinical challenge, and the role of noncoding RNAs in this process has attracted increasing attention. In this study, we found that the long noncoding RNA osteoblast differentiation-related lncRNA under simulated microgravity (ln...
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| Veröffentlicht in: | Cell death & disease 2020-02, Vol.11 (2), p.133-133, Article 133 |
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| container_title | Cell death & disease |
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| creator | Wang, Yixuan Wang, Ke Zhang, Lijun Tan, Yingjun Hu, Zebing Dang, Lei Zhou, Hua Li, Gaozhi Wang, Han Zhang, Shu Shi, Fei Cao, Xinsheng Zhang, Ge |
| description | Ameliorating bone loss caused by mechanical unloading is a substantial clinical challenge, and the role of noncoding RNAs in this process has attracted increasing attention. In this study, we found that the long noncoding RNA osteoblast differentiation-related lncRNA under simulated microgravity (lncRNA ODSM) could inhibit osteoblast apoptosis and promote osteoblast mineralization in vitro. The increased expression level of the lncRNA ODSM partially reduced apoptosis and promoted differentiation in MC3T3-E1 cells under microgravity unloading conditions, and the effect was partially dependent on miR-139-3p. LncRNA ODSM supplementation in hindlimb-unloaded mice caused a decrease in the number of apoptotic cells in bone tissue and an increase in osteoblast activity. Furthermore, targeted overexpression of the lncRNA ODSM in osteoblasts partially reversed bone loss induced by mechanical unloading at the microstructural and biomechanical levels. These findings are the first to suggest the potential value of the lncRNA ODSM in osteoporosis therapy and the treatment of pathological osteopenia. |
| doi_str_mv | 10.1038/s41419-020-2325-3 |
| format | Article |
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In this study, we found that the long noncoding RNA osteoblast differentiation-related lncRNA under simulated microgravity (lncRNA ODSM) could inhibit osteoblast apoptosis and promote osteoblast mineralization in vitro. The increased expression level of the lncRNA ODSM partially reduced apoptosis and promoted differentiation in MC3T3-E1 cells under microgravity unloading conditions, and the effect was partially dependent on miR-139-3p. LncRNA ODSM supplementation in hindlimb-unloaded mice caused a decrease in the number of apoptotic cells in bone tissue and an increase in osteoblast activity. Furthermore, targeted overexpression of the lncRNA ODSM in osteoblasts partially reversed bone loss induced by mechanical unloading at the microstructural and biomechanical levels. These findings are the first to suggest the potential value of the lncRNA ODSM in osteoporosis therapy and the treatment of pathological osteopenia.</description><identifier>ISSN: 2041-4889</identifier><identifier>EISSN: 2041-4889</identifier><identifier>DOI: 10.1038/s41419-020-2325-3</identifier><identifier>PMID: 32071307</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/1 ; 13/109 ; 13/2 ; 13/31 ; 13/89 ; 38/61 ; 38/77 ; 3T3 Cells ; 631/337 ; 64/60 ; 692/699 ; Animals ; Antibodies ; Apoptosis ; Biochemistry ; Biomedical and Life Sciences ; Bone loss ; Cell Biology ; Cell Culture ; Cell Differentiation ; Disease Models, Animal ; ets-Domain Protein Elk-1 - genetics ; ets-Domain Protein Elk-1 - metabolism ; Gene Targeting ; Hindlimb Suspension ; Immunology ; Life Sciences ; Male ; Mechanical unloading ; Mice ; Mice, Inbred C57BL ; Microgravity ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Mineralization ; Osteoblastogenesis ; Osteoblasts ; Osteoblasts - metabolism ; Osteoblasts - pathology ; Osteogenesis ; Osteopenia ; Osteoporosis ; Osteoporosis - genetics ; Osteoporosis - metabolism ; Osteoporosis - pathology ; Osteoporosis - prevention & control ; Ribonucleic acid ; RNA ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Signal Transduction ; Supplements ; Up-Regulation ; Weightlessness Simulation</subject><ispartof>Cell death & disease, 2020-02, Vol.11 (2), p.133-133, Article 133</ispartof><rights>The Author(s) 2020</rights><rights>This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-c9b4901b48decd893a39ca062cc64c51a306e2db213d2b0244bb84ceca7be7303</citedby><cites>FETCH-LOGICAL-c470t-c9b4901b48decd893a39ca062cc64c51a306e2db213d2b0244bb84ceca7be7303</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7028725/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7028725/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32071307$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Yixuan</creatorcontrib><creatorcontrib>Wang, Ke</creatorcontrib><creatorcontrib>Zhang, Lijun</creatorcontrib><creatorcontrib>Tan, Yingjun</creatorcontrib><creatorcontrib>Hu, Zebing</creatorcontrib><creatorcontrib>Dang, Lei</creatorcontrib><creatorcontrib>Zhou, Hua</creatorcontrib><creatorcontrib>Li, Gaozhi</creatorcontrib><creatorcontrib>Wang, Han</creatorcontrib><creatorcontrib>Zhang, Shu</creatorcontrib><creatorcontrib>Shi, Fei</creatorcontrib><creatorcontrib>Cao, Xinsheng</creatorcontrib><creatorcontrib>Zhang, Ge</creatorcontrib><title>Targeted overexpression of the long noncoding RNA ODSM can regulate osteoblast function in vitro and in vivo</title><title>Cell death & disease</title><addtitle>Cell Death Dis</addtitle><addtitle>Cell Death Dis</addtitle><description>Ameliorating bone loss caused by mechanical unloading is a substantial clinical challenge, and the role of noncoding RNAs in this process has attracted increasing attention. In this study, we found that the long noncoding RNA osteoblast differentiation-related lncRNA under simulated microgravity (lncRNA ODSM) could inhibit osteoblast apoptosis and promote osteoblast mineralization in vitro. The increased expression level of the lncRNA ODSM partially reduced apoptosis and promoted differentiation in MC3T3-E1 cells under microgravity unloading conditions, and the effect was partially dependent on miR-139-3p. LncRNA ODSM supplementation in hindlimb-unloaded mice caused a decrease in the number of apoptotic cells in bone tissue and an increase in osteoblast activity. Furthermore, targeted overexpression of the lncRNA ODSM in osteoblasts partially reversed bone loss induced by mechanical unloading at the microstructural and biomechanical levels. These findings are the first to suggest the potential value of the lncRNA ODSM in osteoporosis therapy and the treatment of pathological osteopenia.</description><subject>13/1</subject><subject>13/109</subject><subject>13/2</subject><subject>13/31</subject><subject>13/89</subject><subject>38/61</subject><subject>38/77</subject><subject>3T3 Cells</subject><subject>631/337</subject><subject>64/60</subject><subject>692/699</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Bone loss</subject><subject>Cell Biology</subject><subject>Cell Culture</subject><subject>Cell Differentiation</subject><subject>Disease Models, Animal</subject><subject>ets-Domain Protein Elk-1 - genetics</subject><subject>ets-Domain Protein Elk-1 - metabolism</subject><subject>Gene Targeting</subject><subject>Hindlimb Suspension</subject><subject>Immunology</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Mechanical unloading</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Microgravity</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Mineralization</subject><subject>Osteoblastogenesis</subject><subject>Osteoblasts</subject><subject>Osteoblasts - metabolism</subject><subject>Osteoblasts - pathology</subject><subject>Osteogenesis</subject><subject>Osteopenia</subject><subject>Osteoporosis</subject><subject>Osteoporosis - genetics</subject><subject>Osteoporosis - metabolism</subject><subject>Osteoporosis - pathology</subject><subject>Osteoporosis - prevention & control</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Signal Transduction</subject><subject>Supplements</subject><subject>Up-Regulation</subject><subject>Weightlessness Simulation</subject><issn>2041-4889</issn><issn>2041-4889</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kUtv1TAQhS1ERau2P4ANssSGTWD8SJxskKrylFoqQVlbtjM3TZVrX2znCv49jlJKi4S98FjznWOPDiHPGbxmINo3STLJugo4VFzwuhJPyBEHySrZtt3TB_UhOU3pFsoSAnjdPCOHgoNiAtQRma5NHDBjT8MeI_7cRUxpDJ6GDc03SKfgB-qDd6EfS_X1yxm9evftkjrjacRhnkxGGlLGYCeTMt3M3uVFP3q6H3MM1Ph-vezDCTnYmCnh6d15TL5_eH99_qm6uPr4-fzsonJSQa5cZ2UHzMq2R9e3nTCicwYa7lwjXc2MgAZ5bzkTPbfApbS2lQ6dURaVAHFM3q6-u9lusXfoczST3sVxa-IvHcyoH3f8eKOHsNcKeKt4XQxe3RnE8GPGlPV2TA6nyXgMc9Jc1G3ZCpqCvvwHvQ1z9GW8hVKSiZothmylXAwpRdzcf4aBXuLUa5y6xKmXOLUomhcPp7hX_AmvAHwFUmn5AePfp__v-hvsm6vM</recordid><startdate>20200218</startdate><enddate>20200218</enddate><creator>Wang, Yixuan</creator><creator>Wang, Ke</creator><creator>Zhang, Lijun</creator><creator>Tan, Yingjun</creator><creator>Hu, Zebing</creator><creator>Dang, Lei</creator><creator>Zhou, Hua</creator><creator>Li, Gaozhi</creator><creator>Wang, Han</creator><creator>Zhang, Shu</creator><creator>Shi, Fei</creator><creator>Cao, Xinsheng</creator><creator>Zhang, Ge</creator><general>Nature Publishing Group UK</general><general>Springer Nature B.V</general><scope>C6C</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20200218</creationdate><title>Targeted overexpression of the long noncoding RNA ODSM can regulate osteoblast function in vitro and in vivo</title><author>Wang, Yixuan ; Wang, Ke ; Zhang, Lijun ; Tan, Yingjun ; Hu, Zebing ; Dang, Lei ; Zhou, Hua ; Li, Gaozhi ; Wang, Han ; Zhang, Shu ; Shi, Fei ; Cao, Xinsheng ; Zhang, Ge</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-c9b4901b48decd893a39ca062cc64c51a306e2db213d2b0244bb84ceca7be7303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>13/1</topic><topic>13/109</topic><topic>13/2</topic><topic>13/31</topic><topic>13/89</topic><topic>38/61</topic><topic>38/77</topic><topic>3T3 Cells</topic><topic>631/337</topic><topic>64/60</topic><topic>692/699</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Bone loss</topic><topic>Cell Biology</topic><topic>Cell Culture</topic><topic>Cell Differentiation</topic><topic>Disease Models, Animal</topic><topic>ets-Domain Protein Elk-1 - genetics</topic><topic>ets-Domain Protein Elk-1 - metabolism</topic><topic>Gene Targeting</topic><topic>Hindlimb Suspension</topic><topic>Immunology</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Mechanical unloading</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Microgravity</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Mineralization</topic><topic>Osteoblastogenesis</topic><topic>Osteoblasts</topic><topic>Osteoblasts - metabolism</topic><topic>Osteoblasts - pathology</topic><topic>Osteogenesis</topic><topic>Osteopenia</topic><topic>Osteoporosis</topic><topic>Osteoporosis - genetics</topic><topic>Osteoporosis - metabolism</topic><topic>Osteoporosis - pathology</topic><topic>Osteoporosis - prevention & control</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Signal Transduction</topic><topic>Supplements</topic><topic>Up-Regulation</topic><topic>Weightlessness Simulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Yixuan</creatorcontrib><creatorcontrib>Wang, Ke</creatorcontrib><creatorcontrib>Zhang, Lijun</creatorcontrib><creatorcontrib>Tan, Yingjun</creatorcontrib><creatorcontrib>Hu, Zebing</creatorcontrib><creatorcontrib>Dang, Lei</creatorcontrib><creatorcontrib>Zhou, Hua</creatorcontrib><creatorcontrib>Li, Gaozhi</creatorcontrib><creatorcontrib>Wang, Han</creatorcontrib><creatorcontrib>Zhang, Shu</creatorcontrib><creatorcontrib>Shi, Fei</creatorcontrib><creatorcontrib>Cao, Xinsheng</creatorcontrib><creatorcontrib>Zhang, Ge</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death & disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Yixuan</au><au>Wang, Ke</au><au>Zhang, Lijun</au><au>Tan, Yingjun</au><au>Hu, Zebing</au><au>Dang, Lei</au><au>Zhou, Hua</au><au>Li, Gaozhi</au><au>Wang, Han</au><au>Zhang, Shu</au><au>Shi, Fei</au><au>Cao, Xinsheng</au><au>Zhang, Ge</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Targeted overexpression of the long noncoding RNA ODSM can regulate osteoblast function in vitro and in vivo</atitle><jtitle>Cell death & disease</jtitle><stitle>Cell Death Dis</stitle><addtitle>Cell Death Dis</addtitle><date>2020-02-18</date><risdate>2020</risdate><volume>11</volume><issue>2</issue><spage>133</spage><epage>133</epage><pages>133-133</pages><artnum>133</artnum><issn>2041-4889</issn><eissn>2041-4889</eissn><abstract>Ameliorating bone loss caused by mechanical unloading is a substantial clinical challenge, and the role of noncoding RNAs in this process has attracted increasing attention. In this study, we found that the long noncoding RNA osteoblast differentiation-related lncRNA under simulated microgravity (lncRNA ODSM) could inhibit osteoblast apoptosis and promote osteoblast mineralization in vitro. The increased expression level of the lncRNA ODSM partially reduced apoptosis and promoted differentiation in MC3T3-E1 cells under microgravity unloading conditions, and the effect was partially dependent on miR-139-3p. LncRNA ODSM supplementation in hindlimb-unloaded mice caused a decrease in the number of apoptotic cells in bone tissue and an increase in osteoblast activity. Furthermore, targeted overexpression of the lncRNA ODSM in osteoblasts partially reversed bone loss induced by mechanical unloading at the microstructural and biomechanical levels. These findings are the first to suggest the potential value of the lncRNA ODSM in osteoporosis therapy and the treatment of pathological osteopenia.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>32071307</pmid><doi>10.1038/s41419-020-2325-3</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/1 13/109 13/2 13/31 13/89 38/61 38/77 3T3 Cells 631/337 64/60 692/699 Animals Antibodies Apoptosis Biochemistry Biomedical and Life Sciences Bone loss Cell Biology Cell Culture Cell Differentiation Disease Models, Animal ets-Domain Protein Elk-1 - genetics ets-Domain Protein Elk-1 - metabolism Gene Targeting Hindlimb Suspension Immunology Life Sciences Male Mechanical unloading Mice Mice, Inbred C57BL Microgravity MicroRNAs - genetics MicroRNAs - metabolism Mineralization Osteoblastogenesis Osteoblasts Osteoblasts - metabolism Osteoblasts - pathology Osteogenesis Osteopenia Osteoporosis Osteoporosis - genetics Osteoporosis - metabolism Osteoporosis - pathology Osteoporosis - prevention & control Ribonucleic acid RNA RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Signal Transduction Supplements Up-Regulation Weightlessness Simulation |
| title | Targeted overexpression of the long noncoding RNA ODSM can regulate osteoblast function in vitro and in vivo |
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