Apoptotic Vesicles Regulate Bone Metabolism via the miR1324/SNX14/SMAD1/5 Signaling Axis
Mesenchymal stem cells (MSCs) are widely used in the treatment of diseases. After their in vivo application, MSCs undergo apoptosis and release apoptotic vesicles (apoVs). This study investigates the role of apoVs derived from human bone marrow mesenchymal stem cells (hBMMSCs) in bone metabolism and...
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| Veröffentlicht in: | Small (Weinheim an der Bergstrasse, Germany) Germany), 2023-04, Vol.19 (16), p.e2205813-n/a |
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| creator | Zhu, Yuan Yang, Kunkun Cheng, Yawen Liu, Yaoshan Gu, Ranli Liu, Xuenan Liu, Hao Zhang, Xiao Liu, Yunsong |
| description | Mesenchymal stem cells (MSCs) are widely used in the treatment of diseases. After their in vivo application, MSCs undergo apoptosis and release apoptotic vesicles (apoVs). This study investigates the role of apoVs derived from human bone marrow mesenchymal stem cells (hBMMSCs) in bone metabolism and the molecular mechanism of the observed effects. The results show that apoVs can promote osteogenesis and inhibit osteoclast formation in vitro and in vivo. ApoVs may therefore attenuate the bone loss caused by primary and secondary osteoporosis and stimulate bone regeneration in areas of bone defect. The mechanisms responsible for apoV‐induced bone regeneration include the release of miR1324, which inhibit expression of the target gene Sorting Nexin 14 (SNX14) and thus activate the SMAD1/5 pathway in target cells. Given that MSC‐derived apoVs are easily obtained and stored, with low risks of immunological rejection and neoplastic transformation, The findings suggest a novel therapeutic strategy to treat bone loss, including via cell‐free approaches to bone tissue engineering.
hBMMSC‐apoVs can promote MSC osteogenesis and inhibit osteoclast formation in vitro and in vivo. The mechanisms include the release of miR1324, which inhibits the expression of the target gene SNX14, thereby activating the SMAD1/5 pathway in target cells. The study suggests a novel therapeutic strategy for the treatment of bone loss, including bone tissue engineering through a cell‐free approach. |
| doi_str_mv | 10.1002/smll.202205813 |
| format | Article |
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hBMMSC‐apoVs can promote MSC osteogenesis and inhibit osteoclast formation in vitro and in vivo. The mechanisms include the release of miR1324, which inhibits the expression of the target gene SNX14, thereby activating the SMAD1/5 pathway in target cells. The study suggests a novel therapeutic strategy for the treatment of bone loss, including bone tissue engineering through a cell‐free approach.</description><identifier>ISSN: 1613-6810</identifier><identifier>EISSN: 1613-6829</identifier><identifier>DOI: 10.1002/smll.202205813</identifier><identifier>PMID: 36670083</identifier><language>eng</language><publisher>Germany: Wiley Subscription Services, Inc</publisher><subject>Apoptosis ; apoptotic vesicles ; Bone and Bones ; Bone marrow ; bone metabolism ; Bone Regeneration ; Cell Differentiation - physiology ; cell‐free therapy ; Gene expression ; Humans ; Immunology ; In vivo methods and tests ; Mesenchymal Stem Cells - metabolism ; Metabolism ; miR1324/SNX14/SMAD1/5 signaling axis ; Nanotechnology ; Osteogenesis ; Osteoporosis ; Regeneration (physiology) ; Signal Transduction ; Sorting Nexins - metabolism ; Stem cells ; Tissue engineering ; Vesicles</subject><ispartof>Small (Weinheim an der Bergstrasse, Germany), 2023-04, Vol.19 (16), p.e2205813-n/a</ispartof><rights>2023 Wiley‐VCH GmbH</rights><rights>2023 Wiley-VCH GmbH.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3733-ee2c791133219abce5fd0f4e10bae5fa61a67016a10ea9e97ed82f55fefaf3583</citedby><cites>FETCH-LOGICAL-c3733-ee2c791133219abce5fd0f4e10bae5fa61a67016a10ea9e97ed82f55fefaf3583</cites><orcidid>0000-0003-2069-4487 ; 0000-0001-8364-1898</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fsmll.202205813$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fsmll.202205813$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1413,27906,27907,45556,45557</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36670083$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhu, Yuan</creatorcontrib><creatorcontrib>Yang, Kunkun</creatorcontrib><creatorcontrib>Cheng, Yawen</creatorcontrib><creatorcontrib>Liu, Yaoshan</creatorcontrib><creatorcontrib>Gu, Ranli</creatorcontrib><creatorcontrib>Liu, Xuenan</creatorcontrib><creatorcontrib>Liu, Hao</creatorcontrib><creatorcontrib>Zhang, Xiao</creatorcontrib><creatorcontrib>Liu, Yunsong</creatorcontrib><title>Apoptotic Vesicles Regulate Bone Metabolism via the miR1324/SNX14/SMAD1/5 Signaling Axis</title><title>Small (Weinheim an der Bergstrasse, Germany)</title><addtitle>Small</addtitle><description>Mesenchymal stem cells (MSCs) are widely used in the treatment of diseases. After their in vivo application, MSCs undergo apoptosis and release apoptotic vesicles (apoVs). This study investigates the role of apoVs derived from human bone marrow mesenchymal stem cells (hBMMSCs) in bone metabolism and the molecular mechanism of the observed effects. The results show that apoVs can promote osteogenesis and inhibit osteoclast formation in vitro and in vivo. ApoVs may therefore attenuate the bone loss caused by primary and secondary osteoporosis and stimulate bone regeneration in areas of bone defect. The mechanisms responsible for apoV‐induced bone regeneration include the release of miR1324, which inhibit expression of the target gene Sorting Nexin 14 (SNX14) and thus activate the SMAD1/5 pathway in target cells. Given that MSC‐derived apoVs are easily obtained and stored, with low risks of immunological rejection and neoplastic transformation, The findings suggest a novel therapeutic strategy to treat bone loss, including via cell‐free approaches to bone tissue engineering.
hBMMSC‐apoVs can promote MSC osteogenesis and inhibit osteoclast formation in vitro and in vivo. The mechanisms include the release of miR1324, which inhibits the expression of the target gene SNX14, thereby activating the SMAD1/5 pathway in target cells. The study suggests a novel therapeutic strategy for the treatment of bone loss, including bone tissue engineering through a cell‐free approach.</description><subject>Apoptosis</subject><subject>apoptotic vesicles</subject><subject>Bone and Bones</subject><subject>Bone marrow</subject><subject>bone metabolism</subject><subject>Bone Regeneration</subject><subject>Cell Differentiation - physiology</subject><subject>cell‐free therapy</subject><subject>Gene expression</subject><subject>Humans</subject><subject>Immunology</subject><subject>In vivo methods and tests</subject><subject>Mesenchymal Stem Cells - metabolism</subject><subject>Metabolism</subject><subject>miR1324/SNX14/SMAD1/5 signaling axis</subject><subject>Nanotechnology</subject><subject>Osteogenesis</subject><subject>Osteoporosis</subject><subject>Regeneration (physiology)</subject><subject>Signal Transduction</subject><subject>Sorting Nexins - metabolism</subject><subject>Stem cells</subject><subject>Tissue engineering</subject><subject>Vesicles</subject><issn>1613-6810</issn><issn>1613-6829</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkD1PwzAQhi0EolBYGZElFpa0PjufYymfUgpSC6hb5KSX4sppQpwA_fe4aikSC8vdOzz36vQQcgasB4zxvim07nHGOfNCEHvkCHwQjh_yaH-XgXXIsTELxgRwNzgkHeH7AWOhOCLTQVVWTdmojL6iUZlGQ8c4b7VskF6VS6QjbGRaamUK-qEkbd6QFmoMgrv9yeMU7BwNrqHv0YmaL6VWyzkdfClzQg5yqQ2ebneXvNzePA_vnfjp7mE4iJ1MBEI4iDwLIgAhOEQyzdDLZyx3EVgqbZY-SPsq-BIYygijAGchzz0vx1zmwgtFl1xuequ6fG_RNEmhTIZayyWWrUl4YGW4rh8Ki178QRdlW9ufLRUyHggGkWup3obK6tKYGvOkqlUh61UCLFk7T9bOk51ze3C-rW3TAmc7_EeyBaIN8Kk0rv6pSyajOP4t_wbDeotd</recordid><startdate>20230401</startdate><enddate>20230401</enddate><creator>Zhu, Yuan</creator><creator>Yang, Kunkun</creator><creator>Cheng, Yawen</creator><creator>Liu, Yaoshan</creator><creator>Gu, Ranli</creator><creator>Liu, Xuenan</creator><creator>Liu, Hao</creator><creator>Zhang, Xiao</creator><creator>Liu, Yunsong</creator><general>Wiley Subscription Services, Inc</general><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>7SR</scope><scope>7U5</scope><scope>8BQ</scope><scope>8FD</scope><scope>JG9</scope><scope>L7M</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-2069-4487</orcidid><orcidid>https://orcid.org/0000-0001-8364-1898</orcidid></search><sort><creationdate>20230401</creationdate><title>Apoptotic Vesicles Regulate Bone Metabolism via the miR1324/SNX14/SMAD1/5 Signaling Axis</title><author>Zhu, Yuan ; Yang, Kunkun ; Cheng, Yawen ; Liu, Yaoshan ; Gu, Ranli ; Liu, Xuenan ; Liu, Hao ; Zhang, Xiao ; Liu, Yunsong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3733-ee2c791133219abce5fd0f4e10bae5fa61a67016a10ea9e97ed82f55fefaf3583</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Apoptosis</topic><topic>apoptotic vesicles</topic><topic>Bone and Bones</topic><topic>Bone marrow</topic><topic>bone metabolism</topic><topic>Bone Regeneration</topic><topic>Cell Differentiation - physiology</topic><topic>cell‐free therapy</topic><topic>Gene expression</topic><topic>Humans</topic><topic>Immunology</topic><topic>In vivo methods and tests</topic><topic>Mesenchymal Stem Cells - metabolism</topic><topic>Metabolism</topic><topic>miR1324/SNX14/SMAD1/5 signaling axis</topic><topic>Nanotechnology</topic><topic>Osteogenesis</topic><topic>Osteoporosis</topic><topic>Regeneration (physiology)</topic><topic>Signal Transduction</topic><topic>Sorting Nexins - metabolism</topic><topic>Stem cells</topic><topic>Tissue engineering</topic><topic>Vesicles</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhu, Yuan</creatorcontrib><creatorcontrib>Yang, Kunkun</creatorcontrib><creatorcontrib>Cheng, Yawen</creatorcontrib><creatorcontrib>Liu, Yaoshan</creatorcontrib><creatorcontrib>Gu, Ranli</creatorcontrib><creatorcontrib>Liu, Xuenan</creatorcontrib><creatorcontrib>Liu, Hao</creatorcontrib><creatorcontrib>Zhang, Xiao</creatorcontrib><creatorcontrib>Liu, Yunsong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Engineered Materials Abstracts</collection><collection>Solid State and Superconductivity Abstracts</collection><collection>METADEX</collection><collection>Technology Research Database</collection><collection>Materials Research Database</collection><collection>Advanced Technologies Database with Aerospace</collection><collection>MEDLINE - Academic</collection><jtitle>Small (Weinheim an der Bergstrasse, Germany)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhu, Yuan</au><au>Yang, Kunkun</au><au>Cheng, Yawen</au><au>Liu, Yaoshan</au><au>Gu, Ranli</au><au>Liu, Xuenan</au><au>Liu, Hao</au><au>Zhang, Xiao</au><au>Liu, Yunsong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Apoptotic Vesicles Regulate Bone Metabolism via the miR1324/SNX14/SMAD1/5 Signaling Axis</atitle><jtitle>Small (Weinheim an der Bergstrasse, Germany)</jtitle><addtitle>Small</addtitle><date>2023-04-01</date><risdate>2023</risdate><volume>19</volume><issue>16</issue><spage>e2205813</spage><epage>n/a</epage><pages>e2205813-n/a</pages><issn>1613-6810</issn><eissn>1613-6829</eissn><abstract>Mesenchymal stem cells (MSCs) are widely used in the treatment of diseases. After their in vivo application, MSCs undergo apoptosis and release apoptotic vesicles (apoVs). This study investigates the role of apoVs derived from human bone marrow mesenchymal stem cells (hBMMSCs) in bone metabolism and the molecular mechanism of the observed effects. The results show that apoVs can promote osteogenesis and inhibit osteoclast formation in vitro and in vivo. ApoVs may therefore attenuate the bone loss caused by primary and secondary osteoporosis and stimulate bone regeneration in areas of bone defect. The mechanisms responsible for apoV‐induced bone regeneration include the release of miR1324, which inhibit expression of the target gene Sorting Nexin 14 (SNX14) and thus activate the SMAD1/5 pathway in target cells. Given that MSC‐derived apoVs are easily obtained and stored, with low risks of immunological rejection and neoplastic transformation, The findings suggest a novel therapeutic strategy to treat bone loss, including via cell‐free approaches to bone tissue engineering.
hBMMSC‐apoVs can promote MSC osteogenesis and inhibit osteoclast formation in vitro and in vivo. The mechanisms include the release of miR1324, which inhibits the expression of the target gene SNX14, thereby activating the SMAD1/5 pathway in target cells. The study suggests a novel therapeutic strategy for the treatment of bone loss, including bone tissue engineering through a cell‐free approach.</abstract><cop>Germany</cop><pub>Wiley Subscription Services, Inc</pub><pmid>36670083</pmid><doi>10.1002/smll.202205813</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0003-2069-4487</orcidid><orcidid>https://orcid.org/0000-0001-8364-1898</orcidid></addata></record> |
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| subjects | Apoptosis apoptotic vesicles Bone and Bones Bone marrow bone metabolism Bone Regeneration Cell Differentiation - physiology cell‐free therapy Gene expression Humans Immunology In vivo methods and tests Mesenchymal Stem Cells - metabolism Metabolism miR1324/SNX14/SMAD1/5 signaling axis Nanotechnology Osteogenesis Osteoporosis Regeneration (physiology) Signal Transduction Sorting Nexins - metabolism Stem cells Tissue engineering Vesicles |
| title | Apoptotic Vesicles Regulate Bone Metabolism via the miR1324/SNX14/SMAD1/5 Signaling Axis |
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