Cyclooxygenase 2 augments osteoblastic but suppresses chondrocytic differentiation of CD90 + skeletal stem cells in fracture sites
Cyclooxygenase 2 (COX-2) is essential for normal tissue repair. Although COX-2 is known to enhance the differentiation of mesenchymal stem cells (MSCs), how COX-2 regulates MSC differentiation into different tissue-specific progenitors to promote tissue repair remains unknown. Because it has been sh...
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| Veröffentlicht in: | Science advances 2019-07, Vol.5 (7), p.eaaw2108-eaaw2108 |
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| creator | Wasnik, Samiksha Lakhan, Ram Baylink, David J Rundle, Charles H Xu, Yi Zhang, Jintao Qin, Xuezhong Lau, Kin-Hing William Carreon, Edmundo E Tang, Xiaolei |
| description | Cyclooxygenase 2 (COX-2) is essential for normal tissue repair. Although COX-2 is known to enhance the differentiation of mesenchymal stem cells (MSCs), how COX-2 regulates MSC differentiation into different tissue-specific progenitors to promote tissue repair remains unknown. Because it has been shown that COX-2 is critical for normal bone repair and local COX-2 overexpression in fracture sites accelerates fracture repair, this study aimed to determine the MSC subsets that are targeted by COX-2. We showed that CD90
mouse skeletal stem cells (mSSCs; i.e., CD45
Tie2
AlphaV
MSCs) were selectively recruited by macrophage/monocyte chemoattractant protein 1 into fracture sites following local COX-2 overexpression. In addition, local COX-2 overexpression augmented osteoblast differentiation and suppressed chondrocyte differentiation in CD90
mSSCs, which depended on canonical WNT signaling. CD90 depletion data demonstrated that local COX-2 overexpression targeted CD90
mSSCs to accelerate fracture repair. In conclusion, CD90
mSSCs are promising targets for the acceleration of bone repair. |
| doi_str_mv | 10.1126/sciadv.aaw2108 |
| format | Article |
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mouse skeletal stem cells (mSSCs; i.e., CD45
Tie2
AlphaV
MSCs) were selectively recruited by macrophage/monocyte chemoattractant protein 1 into fracture sites following local COX-2 overexpression. In addition, local COX-2 overexpression augmented osteoblast differentiation and suppressed chondrocyte differentiation in CD90
mSSCs, which depended on canonical WNT signaling. CD90 depletion data demonstrated that local COX-2 overexpression targeted CD90
mSSCs to accelerate fracture repair. In conclusion, CD90
mSSCs are promising targets for the acceleration of bone repair.</description><identifier>ISSN: 2375-2548</identifier><identifier>EISSN: 2375-2548</identifier><identifier>DOI: 10.1126/sciadv.aaw2108</identifier><identifier>PMID: 31392271</identifier><language>eng</language><publisher>United States: American Association for the Advancement of Science</publisher><subject>Animals ; Bone Regeneration - genetics ; Cell Biology ; Cell Differentiation - genetics ; Chondrocytes - cytology ; Cyclooxygenase 2 - genetics ; Fractures, Bone - genetics ; Fractures, Bone - pathology ; Gene Expression Regulation, Developmental - genetics ; Humans ; Leukocyte Common Antigens - genetics ; Mesenchymal Stem Cells - cytology ; Mice ; Osteoblasts - cytology ; Osteogenesis - genetics ; Receptor, TIE-2 - genetics ; SciAdv r-articles ; Thy-1 Antigens - genetics ; Wnt Signaling Pathway - genetics</subject><ispartof>Science advances, 2019-07, Vol.5 (7), p.eaaw2108-eaaw2108</ispartof><rights>Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC). 2019 The Authors</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-b02a0b904e7f57853acba35b72eb41dfdafff4c0a3096efa8492fbd3a322935b3</citedby><cites>FETCH-LOGICAL-c390t-b02a0b904e7f57853acba35b72eb41dfdafff4c0a3096efa8492fbd3a322935b3</cites><orcidid>0000-0002-2700-6272 ; 0000-0003-1109-5052 ; 0000-0003-1492-9622 ; 0000-0001-6097-0517</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6669009/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6669009/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31392271$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wasnik, Samiksha</creatorcontrib><creatorcontrib>Lakhan, Ram</creatorcontrib><creatorcontrib>Baylink, David J</creatorcontrib><creatorcontrib>Rundle, Charles H</creatorcontrib><creatorcontrib>Xu, Yi</creatorcontrib><creatorcontrib>Zhang, Jintao</creatorcontrib><creatorcontrib>Qin, Xuezhong</creatorcontrib><creatorcontrib>Lau, Kin-Hing William</creatorcontrib><creatorcontrib>Carreon, Edmundo E</creatorcontrib><creatorcontrib>Tang, Xiaolei</creatorcontrib><title>Cyclooxygenase 2 augments osteoblastic but suppresses chondrocytic differentiation of CD90 + skeletal stem cells in fracture sites</title><title>Science advances</title><addtitle>Sci Adv</addtitle><description>Cyclooxygenase 2 (COX-2) is essential for normal tissue repair. Although COX-2 is known to enhance the differentiation of mesenchymal stem cells (MSCs), how COX-2 regulates MSC differentiation into different tissue-specific progenitors to promote tissue repair remains unknown. Because it has been shown that COX-2 is critical for normal bone repair and local COX-2 overexpression in fracture sites accelerates fracture repair, this study aimed to determine the MSC subsets that are targeted by COX-2. We showed that CD90
mouse skeletal stem cells (mSSCs; i.e., CD45
Tie2
AlphaV
MSCs) were selectively recruited by macrophage/monocyte chemoattractant protein 1 into fracture sites following local COX-2 overexpression. In addition, local COX-2 overexpression augmented osteoblast differentiation and suppressed chondrocyte differentiation in CD90
mSSCs, which depended on canonical WNT signaling. CD90 depletion data demonstrated that local COX-2 overexpression targeted CD90
mSSCs to accelerate fracture repair. In conclusion, CD90
mSSCs are promising targets for the acceleration of bone repair.</description><subject>Animals</subject><subject>Bone Regeneration - genetics</subject><subject>Cell Biology</subject><subject>Cell Differentiation - genetics</subject><subject>Chondrocytes - cytology</subject><subject>Cyclooxygenase 2 - genetics</subject><subject>Fractures, Bone - genetics</subject><subject>Fractures, Bone - pathology</subject><subject>Gene Expression Regulation, Developmental - genetics</subject><subject>Humans</subject><subject>Leukocyte Common Antigens - genetics</subject><subject>Mesenchymal Stem Cells - cytology</subject><subject>Mice</subject><subject>Osteoblasts - cytology</subject><subject>Osteogenesis - genetics</subject><subject>Receptor, TIE-2 - genetics</subject><subject>SciAdv r-articles</subject><subject>Thy-1 Antigens - genetics</subject><subject>Wnt Signaling Pathway - genetics</subject><issn>2375-2548</issn><issn>2375-2548</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUU2LFDEQDaK4y7pXj5KjIDPmoz8mF0HGT1jwoudQSVdmo92dMZVenau_3AwzLuupCt6rV1XvMfZcirWUqntNPsJwtwb4paTYPGKXSvftSrXN5vGD_oJdE30XQsim61ppnrILLbVRqpeX7M_24MeUfh92OAMhVxyW3YRzIZ6oYHIjUImeu6VwWvb7jERI3N-mecjJH47YEEPAXGcilJhmngLfvjOCv-L0A0csMPIqNXGP40g8zjxk8GXJyCkWpGfsSYCR8Ppcr9i3D--_bj-tbr58_Lx9e7Py2oiyckKBcEY02Ie237QavAPdul6ha-QQBgghNF6AFqbDAJvGqOAGDVopU3n6ir056e4XN-Hg68EZRrvPcYJ8sAmi_R-Z463dpTvbdZ0RwlSBl2eBnH4uSMVOkY5PwYxpIVsdrSa3XaMqdX2i-pyIMob7NVLYY3b2lJ09Z1cHXjw87p7-Lyn9FzRdm7Y</recordid><startdate>20190701</startdate><enddate>20190701</enddate><creator>Wasnik, Samiksha</creator><creator>Lakhan, Ram</creator><creator>Baylink, David J</creator><creator>Rundle, Charles H</creator><creator>Xu, Yi</creator><creator>Zhang, Jintao</creator><creator>Qin, Xuezhong</creator><creator>Lau, Kin-Hing William</creator><creator>Carreon, Edmundo E</creator><creator>Tang, Xiaolei</creator><general>American Association for the Advancement of Science</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>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-2700-6272</orcidid><orcidid>https://orcid.org/0000-0003-1109-5052</orcidid><orcidid>https://orcid.org/0000-0003-1492-9622</orcidid><orcidid>https://orcid.org/0000-0001-6097-0517</orcidid></search><sort><creationdate>20190701</creationdate><title>Cyclooxygenase 2 augments osteoblastic but suppresses chondrocytic differentiation of CD90 + skeletal stem cells in fracture sites</title><author>Wasnik, Samiksha ; Lakhan, Ram ; Baylink, David J ; Rundle, Charles H ; Xu, Yi ; Zhang, Jintao ; Qin, Xuezhong ; Lau, Kin-Hing William ; Carreon, Edmundo E ; Tang, Xiaolei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-b02a0b904e7f57853acba35b72eb41dfdafff4c0a3096efa8492fbd3a322935b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Bone Regeneration - genetics</topic><topic>Cell Biology</topic><topic>Cell Differentiation - genetics</topic><topic>Chondrocytes - cytology</topic><topic>Cyclooxygenase 2 - genetics</topic><topic>Fractures, Bone - genetics</topic><topic>Fractures, Bone - pathology</topic><topic>Gene Expression Regulation, Developmental - genetics</topic><topic>Humans</topic><topic>Leukocyte Common Antigens - genetics</topic><topic>Mesenchymal Stem Cells - cytology</topic><topic>Mice</topic><topic>Osteoblasts - cytology</topic><topic>Osteogenesis - genetics</topic><topic>Receptor, TIE-2 - genetics</topic><topic>SciAdv r-articles</topic><topic>Thy-1 Antigens - genetics</topic><topic>Wnt Signaling Pathway - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wasnik, Samiksha</creatorcontrib><creatorcontrib>Lakhan, Ram</creatorcontrib><creatorcontrib>Baylink, David J</creatorcontrib><creatorcontrib>Rundle, Charles H</creatorcontrib><creatorcontrib>Xu, Yi</creatorcontrib><creatorcontrib>Zhang, Jintao</creatorcontrib><creatorcontrib>Qin, Xuezhong</creatorcontrib><creatorcontrib>Lau, Kin-Hing William</creatorcontrib><creatorcontrib>Carreon, Edmundo E</creatorcontrib><creatorcontrib>Tang, Xiaolei</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Science advances</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wasnik, Samiksha</au><au>Lakhan, Ram</au><au>Baylink, David J</au><au>Rundle, Charles H</au><au>Xu, Yi</au><au>Zhang, Jintao</au><au>Qin, Xuezhong</au><au>Lau, Kin-Hing William</au><au>Carreon, Edmundo E</au><au>Tang, Xiaolei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cyclooxygenase 2 augments osteoblastic but suppresses chondrocytic differentiation of CD90 + skeletal stem cells in fracture sites</atitle><jtitle>Science advances</jtitle><addtitle>Sci Adv</addtitle><date>2019-07-01</date><risdate>2019</risdate><volume>5</volume><issue>7</issue><spage>eaaw2108</spage><epage>eaaw2108</epage><pages>eaaw2108-eaaw2108</pages><issn>2375-2548</issn><eissn>2375-2548</eissn><abstract>Cyclooxygenase 2 (COX-2) is essential for normal tissue repair. Although COX-2 is known to enhance the differentiation of mesenchymal stem cells (MSCs), how COX-2 regulates MSC differentiation into different tissue-specific progenitors to promote tissue repair remains unknown. Because it has been shown that COX-2 is critical for normal bone repair and local COX-2 overexpression in fracture sites accelerates fracture repair, this study aimed to determine the MSC subsets that are targeted by COX-2. We showed that CD90
mouse skeletal stem cells (mSSCs; i.e., CD45
Tie2
AlphaV
MSCs) were selectively recruited by macrophage/monocyte chemoattractant protein 1 into fracture sites following local COX-2 overexpression. In addition, local COX-2 overexpression augmented osteoblast differentiation and suppressed chondrocyte differentiation in CD90
mSSCs, which depended on canonical WNT signaling. CD90 depletion data demonstrated that local COX-2 overexpression targeted CD90
mSSCs to accelerate fracture repair. In conclusion, CD90
mSSCs are promising targets for the acceleration of bone repair.</abstract><cop>United States</cop><pub>American Association for the Advancement of Science</pub><pmid>31392271</pmid><doi>10.1126/sciadv.aaw2108</doi><orcidid>https://orcid.org/0000-0002-2700-6272</orcidid><orcidid>https://orcid.org/0000-0003-1109-5052</orcidid><orcidid>https://orcid.org/0000-0003-1492-9622</orcidid><orcidid>https://orcid.org/0000-0001-6097-0517</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Animals Bone Regeneration - genetics Cell Biology Cell Differentiation - genetics Chondrocytes - cytology Cyclooxygenase 2 - genetics Fractures, Bone - genetics Fractures, Bone - pathology Gene Expression Regulation, Developmental - genetics Humans Leukocyte Common Antigens - genetics Mesenchymal Stem Cells - cytology Mice Osteoblasts - cytology Osteogenesis - genetics Receptor, TIE-2 - genetics SciAdv r-articles Thy-1 Antigens - genetics Wnt Signaling Pathway - genetics |
| title | Cyclooxygenase 2 augments osteoblastic but suppresses chondrocytic differentiation of CD90 + skeletal stem cells in fracture sites |
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