Macrophage-Derived Extracellular DNA Initiates Heterotopic Ossification
Heterotopic ossification (HO) severely affects people's lives; however, its pathological mechanism remains poorly understood. Although extracellular DNA (ecDNA) has been shown to play important roles in pathological calcification, its effects in HO development and progression remain unknown. Th...
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| Veröffentlicht in: | Inflammation 2023-12, Vol.46 (6), p.2225-2240 |
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| creator | Han, Xiaoxiao Gao, Changhe Lu, Weicheng Yan, Jianfei Xu, Haoqing Guo, Zhenxing Qin, Wenpin Lu, Naining Gao, Jialu Zhu, Weiwei Fu, Yutong Jiao, Kai |
| description | Heterotopic ossification (HO) severely affects people's lives; however, its pathological mechanism remains poorly understood. Although extracellular DNA (ecDNA) has been shown to play important roles in pathological calcification, its effects in HO development and progression remain unknown. The
in vivo
rat Achilles tendon injury model and i
n vitro
collagen I calcification model were used to evaluate the effects of ecDNA in the ectopic calcifications and the main cell types involved in those pathological process. Histology, immunofluorescent staining, reverse transcriptase-polymerase chain reaction analysis and micro-computed tomography were used to identify the distribution of macrophage-derived ecDNA and elucidate their roles in HO. The results showed that the amount of ecDNA and ectopic calcification increased significantly and exhibited a strong correlation in the injured tendons of HO model compared with those of the controls, which was accompanied by a significantly increased number of M2 macrophages in the injured tendon. During
in vitro
co-culture experiments, M2 macrophages calcified the reconstituted type I collagen and ectopic bone collected from the injured tendons of HO rats, while those effects were inhibited by deoxyribonuclease. More importantly, deoxyribonuclease reversed the pathological calcification in the injured rat tendon HO model. The present study showed that ecDNA from M2 macrophages initiates pathological calcification in HO, and the elimination of ecDNA might be developed into a clinical strategy to prevent ectopic mineralization diseases. The use of deoxyribonuclease for the targeted degradation of ecDNA at affected tissue sites provides a potential solution to treat diseases associated with ectopic mineralization. |
| doi_str_mv | 10.1007/s10753-023-01873-8 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2839246769</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2839246769</sourcerecordid><originalsourceid>FETCH-LOGICAL-c370t-e83b20a59233918aff3b6959e1c5b7296438f56c5b069844da8ccca54d37afba3</originalsourceid><addsrcrecordid>eNp9kD1PwzAQhi0EoqXwBxhQJBaWgO2Lv0bU8iUVusBsOY4DRm1S7ATBv8eQAhIDg3W27rnXpwehQ4JPCcbiLBIsGOSYpkOkgFxuoTFh6UKZ4NtojIHjHJQSI7QX4zPGWCoJu2gEomBSETVGV7fGhnb9ZB5dPnPBv7oqu3jrgrFuueyXJmSzu_PspvGdN52L2bXrXGi7du1ttojR196azrfNPtqpzTK6g02doIfLi_vpdT5fXN1Mz-e5BYG73EkoKTZMUQBFpKlrKLliyhHLSkEVL0DWjKcH5koWRWWktdawogJh6tLABJ0MuevQvvQudnrl4-eupnFtHzWVoGjBBVcJPf6DPrd9aNJ2iVJAJWacJIoOVNIQY3C1Xge_MuFdE6w_NetBs06a9ZdmLdPQ0Sa6L1eu-hn59poAGICYWs2jC79__xP7AaYph0U</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2893280561</pqid></control><display><type>article</type><title>Macrophage-Derived Extracellular DNA Initiates Heterotopic Ossification</title><source>SpringerNature Journals</source><creator>Han, Xiaoxiao ; Gao, Changhe ; Lu, Weicheng ; Yan, Jianfei ; Xu, Haoqing ; Guo, Zhenxing ; Qin, Wenpin ; Lu, Naining ; Gao, Jialu ; Zhu, Weiwei ; Fu, Yutong ; Jiao, Kai</creator><creatorcontrib>Han, Xiaoxiao ; Gao, Changhe ; Lu, Weicheng ; Yan, Jianfei ; Xu, Haoqing ; Guo, Zhenxing ; Qin, Wenpin ; Lu, Naining ; Gao, Jialu ; Zhu, Weiwei ; Fu, Yutong ; Jiao, Kai</creatorcontrib><description>Heterotopic ossification (HO) severely affects people's lives; however, its pathological mechanism remains poorly understood. Although extracellular DNA (ecDNA) has been shown to play important roles in pathological calcification, its effects in HO development and progression remain unknown. The
in vivo
rat Achilles tendon injury model and i
n vitro
collagen I calcification model were used to evaluate the effects of ecDNA in the ectopic calcifications and the main cell types involved in those pathological process. Histology, immunofluorescent staining, reverse transcriptase-polymerase chain reaction analysis and micro-computed tomography were used to identify the distribution of macrophage-derived ecDNA and elucidate their roles in HO. The results showed that the amount of ecDNA and ectopic calcification increased significantly and exhibited a strong correlation in the injured tendons of HO model compared with those of the controls, which was accompanied by a significantly increased number of M2 macrophages in the injured tendon. During
in vitro
co-culture experiments, M2 macrophages calcified the reconstituted type I collagen and ectopic bone collected from the injured tendons of HO rats, while those effects were inhibited by deoxyribonuclease. More importantly, deoxyribonuclease reversed the pathological calcification in the injured rat tendon HO model. The present study showed that ecDNA from M2 macrophages initiates pathological calcification in HO, and the elimination of ecDNA might be developed into a clinical strategy to prevent ectopic mineralization diseases. The use of deoxyribonuclease for the targeted degradation of ecDNA at affected tissue sites provides a potential solution to treat diseases associated with ectopic mineralization.</description><identifier>ISSN: 0360-3997</identifier><identifier>EISSN: 1573-2576</identifier><identifier>DOI: 10.1007/s10753-023-01873-8</identifier><identifier>PMID: 37458919</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Achilles tendon ; Biomedical and Life Sciences ; Biomedicine ; Calcification ; Calcification (ectopic) ; Cell culture ; Collagen (type I) ; Computed tomography ; Deoxyribonuclease ; Immunology ; Internal Medicine ; Macrophages ; Mineralization ; Ossification (ectopic) ; Pathology ; Pharmacology/Toxicology ; Rheumatology ; RNA-directed DNA polymerase ; Tendons</subject><ispartof>Inflammation, 2023-12, Vol.46 (6), p.2225-2240</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c370t-e83b20a59233918aff3b6959e1c5b7296438f56c5b069844da8ccca54d37afba3</cites><orcidid>0000-0002-4838-810X ; 0000-0002-3016-5047 ; 0000-0003-3669-8095 ; 0000-0002-6453-5034 ; 0009-0005-5792-8592 ; 0000-0002-1901-8329 ; 0000-0003-4071-895X ; 0009-0002-0959-0118 ; 0009-0002-9889-346X ; 0000-0002-9252-0657 ; 0000-0002-3945-737X ; 0009-0001-7450-0353</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10753-023-01873-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10753-023-01873-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27928,27929,41492,42561,51323</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37458919$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Han, Xiaoxiao</creatorcontrib><creatorcontrib>Gao, Changhe</creatorcontrib><creatorcontrib>Lu, Weicheng</creatorcontrib><creatorcontrib>Yan, Jianfei</creatorcontrib><creatorcontrib>Xu, Haoqing</creatorcontrib><creatorcontrib>Guo, Zhenxing</creatorcontrib><creatorcontrib>Qin, Wenpin</creatorcontrib><creatorcontrib>Lu, Naining</creatorcontrib><creatorcontrib>Gao, Jialu</creatorcontrib><creatorcontrib>Zhu, Weiwei</creatorcontrib><creatorcontrib>Fu, Yutong</creatorcontrib><creatorcontrib>Jiao, Kai</creatorcontrib><title>Macrophage-Derived Extracellular DNA Initiates Heterotopic Ossification</title><title>Inflammation</title><addtitle>Inflammation</addtitle><addtitle>Inflammation</addtitle><description>Heterotopic ossification (HO) severely affects people's lives; however, its pathological mechanism remains poorly understood. Although extracellular DNA (ecDNA) has been shown to play important roles in pathological calcification, its effects in HO development and progression remain unknown. The
in vivo
rat Achilles tendon injury model and i
n vitro
collagen I calcification model were used to evaluate the effects of ecDNA in the ectopic calcifications and the main cell types involved in those pathological process. Histology, immunofluorescent staining, reverse transcriptase-polymerase chain reaction analysis and micro-computed tomography were used to identify the distribution of macrophage-derived ecDNA and elucidate their roles in HO. The results showed that the amount of ecDNA and ectopic calcification increased significantly and exhibited a strong correlation in the injured tendons of HO model compared with those of the controls, which was accompanied by a significantly increased number of M2 macrophages in the injured tendon. During
in vitro
co-culture experiments, M2 macrophages calcified the reconstituted type I collagen and ectopic bone collected from the injured tendons of HO rats, while those effects were inhibited by deoxyribonuclease. More importantly, deoxyribonuclease reversed the pathological calcification in the injured rat tendon HO model. The present study showed that ecDNA from M2 macrophages initiates pathological calcification in HO, and the elimination of ecDNA might be developed into a clinical strategy to prevent ectopic mineralization diseases. The use of deoxyribonuclease for the targeted degradation of ecDNA at affected tissue sites provides a potential solution to treat diseases associated with ectopic mineralization.</description><subject>Achilles tendon</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Calcification</subject><subject>Calcification (ectopic)</subject><subject>Cell culture</subject><subject>Collagen (type I)</subject><subject>Computed tomography</subject><subject>Deoxyribonuclease</subject><subject>Immunology</subject><subject>Internal Medicine</subject><subject>Macrophages</subject><subject>Mineralization</subject><subject>Ossification (ectopic)</subject><subject>Pathology</subject><subject>Pharmacology/Toxicology</subject><subject>Rheumatology</subject><subject>RNA-directed DNA polymerase</subject><subject>Tendons</subject><issn>0360-3997</issn><issn>1573-2576</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kD1PwzAQhi0EoqXwBxhQJBaWgO2Lv0bU8iUVusBsOY4DRm1S7ATBv8eQAhIDg3W27rnXpwehQ4JPCcbiLBIsGOSYpkOkgFxuoTFh6UKZ4NtojIHjHJQSI7QX4zPGWCoJu2gEomBSETVGV7fGhnb9ZB5dPnPBv7oqu3jrgrFuueyXJmSzu_PspvGdN52L2bXrXGi7du1ttojR196azrfNPtqpzTK6g02doIfLi_vpdT5fXN1Mz-e5BYG73EkoKTZMUQBFpKlrKLliyhHLSkEVL0DWjKcH5koWRWWktdawogJh6tLABJ0MuevQvvQudnrl4-eupnFtHzWVoGjBBVcJPf6DPrd9aNJ2iVJAJWacJIoOVNIQY3C1Xge_MuFdE6w_NetBs06a9ZdmLdPQ0Sa6L1eu-hn59poAGICYWs2jC79__xP7AaYph0U</recordid><startdate>20231201</startdate><enddate>20231201</enddate><creator>Han, Xiaoxiao</creator><creator>Gao, Changhe</creator><creator>Lu, Weicheng</creator><creator>Yan, Jianfei</creator><creator>Xu, Haoqing</creator><creator>Guo, Zhenxing</creator><creator>Qin, Wenpin</creator><creator>Lu, Naining</creator><creator>Gao, Jialu</creator><creator>Zhu, Weiwei</creator><creator>Fu, Yutong</creator><creator>Jiao, Kai</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4838-810X</orcidid><orcidid>https://orcid.org/0000-0002-3016-5047</orcidid><orcidid>https://orcid.org/0000-0003-3669-8095</orcidid><orcidid>https://orcid.org/0000-0002-6453-5034</orcidid><orcidid>https://orcid.org/0009-0005-5792-8592</orcidid><orcidid>https://orcid.org/0000-0002-1901-8329</orcidid><orcidid>https://orcid.org/0000-0003-4071-895X</orcidid><orcidid>https://orcid.org/0009-0002-0959-0118</orcidid><orcidid>https://orcid.org/0009-0002-9889-346X</orcidid><orcidid>https://orcid.org/0000-0002-9252-0657</orcidid><orcidid>https://orcid.org/0000-0002-3945-737X</orcidid><orcidid>https://orcid.org/0009-0001-7450-0353</orcidid></search><sort><creationdate>20231201</creationdate><title>Macrophage-Derived Extracellular DNA Initiates Heterotopic Ossification</title><author>Han, Xiaoxiao ; Gao, Changhe ; Lu, Weicheng ; Yan, Jianfei ; Xu, Haoqing ; Guo, Zhenxing ; Qin, Wenpin ; Lu, Naining ; Gao, Jialu ; Zhu, Weiwei ; Fu, Yutong ; Jiao, Kai</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c370t-e83b20a59233918aff3b6959e1c5b7296438f56c5b069844da8ccca54d37afba3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Achilles tendon</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Calcification</topic><topic>Calcification (ectopic)</topic><topic>Cell culture</topic><topic>Collagen (type I)</topic><topic>Computed tomography</topic><topic>Deoxyribonuclease</topic><topic>Immunology</topic><topic>Internal Medicine</topic><topic>Macrophages</topic><topic>Mineralization</topic><topic>Ossification (ectopic)</topic><topic>Pathology</topic><topic>Pharmacology/Toxicology</topic><topic>Rheumatology</topic><topic>RNA-directed DNA polymerase</topic><topic>Tendons</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Han, Xiaoxiao</creatorcontrib><creatorcontrib>Gao, Changhe</creatorcontrib><creatorcontrib>Lu, Weicheng</creatorcontrib><creatorcontrib>Yan, Jianfei</creatorcontrib><creatorcontrib>Xu, Haoqing</creatorcontrib><creatorcontrib>Guo, Zhenxing</creatorcontrib><creatorcontrib>Qin, Wenpin</creatorcontrib><creatorcontrib>Lu, Naining</creatorcontrib><creatorcontrib>Gao, Jialu</creatorcontrib><creatorcontrib>Zhu, Weiwei</creatorcontrib><creatorcontrib>Fu, Yutong</creatorcontrib><creatorcontrib>Jiao, Kai</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma 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</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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>MEDLINE - Academic</collection><jtitle>Inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Han, Xiaoxiao</au><au>Gao, Changhe</au><au>Lu, Weicheng</au><au>Yan, Jianfei</au><au>Xu, Haoqing</au><au>Guo, Zhenxing</au><au>Qin, Wenpin</au><au>Lu, Naining</au><au>Gao, Jialu</au><au>Zhu, Weiwei</au><au>Fu, Yutong</au><au>Jiao, Kai</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Macrophage-Derived Extracellular DNA Initiates Heterotopic Ossification</atitle><jtitle>Inflammation</jtitle><stitle>Inflammation</stitle><addtitle>Inflammation</addtitle><date>2023-12-01</date><risdate>2023</risdate><volume>46</volume><issue>6</issue><spage>2225</spage><epage>2240</epage><pages>2225-2240</pages><issn>0360-3997</issn><eissn>1573-2576</eissn><abstract>Heterotopic ossification (HO) severely affects people's lives; however, its pathological mechanism remains poorly understood. Although extracellular DNA (ecDNA) has been shown to play important roles in pathological calcification, its effects in HO development and progression remain unknown. The
in vivo
rat Achilles tendon injury model and i
n vitro
collagen I calcification model were used to evaluate the effects of ecDNA in the ectopic calcifications and the main cell types involved in those pathological process. Histology, immunofluorescent staining, reverse transcriptase-polymerase chain reaction analysis and micro-computed tomography were used to identify the distribution of macrophage-derived ecDNA and elucidate their roles in HO. The results showed that the amount of ecDNA and ectopic calcification increased significantly and exhibited a strong correlation in the injured tendons of HO model compared with those of the controls, which was accompanied by a significantly increased number of M2 macrophages in the injured tendon. During
in vitro
co-culture experiments, M2 macrophages calcified the reconstituted type I collagen and ectopic bone collected from the injured tendons of HO rats, while those effects were inhibited by deoxyribonuclease. More importantly, deoxyribonuclease reversed the pathological calcification in the injured rat tendon HO model. The present study showed that ecDNA from M2 macrophages initiates pathological calcification in HO, and the elimination of ecDNA might be developed into a clinical strategy to prevent ectopic mineralization diseases. The use of deoxyribonuclease for the targeted degradation of ecDNA at affected tissue sites provides a potential solution to treat diseases associated with ectopic mineralization.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>37458919</pmid><doi>10.1007/s10753-023-01873-8</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0002-4838-810X</orcidid><orcidid>https://orcid.org/0000-0002-3016-5047</orcidid><orcidid>https://orcid.org/0000-0003-3669-8095</orcidid><orcidid>https://orcid.org/0000-0002-6453-5034</orcidid><orcidid>https://orcid.org/0009-0005-5792-8592</orcidid><orcidid>https://orcid.org/0000-0002-1901-8329</orcidid><orcidid>https://orcid.org/0000-0003-4071-895X</orcidid><orcidid>https://orcid.org/0009-0002-0959-0118</orcidid><orcidid>https://orcid.org/0009-0002-9889-346X</orcidid><orcidid>https://orcid.org/0000-0002-9252-0657</orcidid><orcidid>https://orcid.org/0000-0002-3945-737X</orcidid><orcidid>https://orcid.org/0009-0001-7450-0353</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Achilles tendon Biomedical and Life Sciences Biomedicine Calcification Calcification (ectopic) Cell culture Collagen (type I) Computed tomography Deoxyribonuclease Immunology Internal Medicine Macrophages Mineralization Ossification (ectopic) Pathology Pharmacology/Toxicology Rheumatology RNA-directed DNA polymerase Tendons |
| title | Macrophage-Derived Extracellular DNA Initiates Heterotopic Ossification |
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