LncRNA Neat1 promotes the macrophage inflammatory response and acts as a therapeutic target in titanium particle-induced osteolysis
Aseptic loosening (AL), secondary to particle-caused periprosthetic osteolysis, is one of the main reasons of artificial joint failure. Suppressing the macrophage inflammatory response caused by wear particles extends the life of prosthesis, and the long noncoding RNAs (lncRNAs) may play a predomina...
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| Veröffentlicht in: | Acta biomaterialia 2022-04, Vol.142, p.345-360 |
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| creator | Lin, Sipeng Wen, Zhenkang Li, Shixun Chen, Zhong Li, Changchuan Ouyang, Zhuji Lin, Chuangxin Kuang, Manyuan Xue, Chunyu Ding, Yue |
| description | Aseptic loosening (AL), secondary to particle-caused periprosthetic osteolysis, is one of the main reasons of artificial joint failure. Suppressing the macrophage inflammatory response caused by wear particles extends the life of prosthesis, and the long noncoding RNAs (lncRNAs) may play a predominant part in it. Here, titanium particles’ (TiPs’) stimulation increases both the cytoplasmic and nuclear levels of lncRNA Neat1 in bone marrow derived macrophages (BMDMs), which further induces the inflammatory response. Mechanically, Neat1 facilitates Bruton's tyrosine kinase (BTK) transcription by reducing the transcriptional factor KLF4, which further activates the NF-κB pathway, NLRP3 inflammation, and M1 polarization in BMDMs. Cytoplasmic Neat1 also works as an miRNA sponge in miR-188–5p-regulated BTK expression in the post-transcriptional stage. In vivo, Neat1 downregulation can reduce the TiP-induced pro-inflammatory factors and reverse the osteolysis induced by BTK overexpression. In addition, the PLGA-based microparticles loaded with si-Neat1 are developed for the treatment of the mouse calvarial osteolysis model via local injection, presenting satisfactory anti-osteolysis efficacy. These findings indicate that Neat1 is a key regulator of AL.
Due to released particles, aseptic loosening (AL) is the most common reason for prosthesis failure and surgical revision and represents a substantial economic burden worldwide. Herein, we reported that lncRNA Neat1 is a key regulator in regulating wear particles-induced osteolysis by activating NF-κB pathway, NLRP3 inflammation and M1 polarization via BTK, and the underlying mechanisms of Neat1-BTK interaction were further portrayed. For potential clinical application, the microparticles are developed for effective si-Neat1 delivery, leading to a dramatically enhanced effect for the treatment of osteolysis, which might be a novel strategy to extend the life of the implant.
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| doi_str_mv | 10.1016/j.actbio.2022.02.007 |
| format | Article |
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Due to released particles, aseptic loosening (AL) is the most common reason for prosthesis failure and surgical revision and represents a substantial economic burden worldwide. Herein, we reported that lncRNA Neat1 is a key regulator in regulating wear particles-induced osteolysis by activating NF-κB pathway, NLRP3 inflammation and M1 polarization via BTK, and the underlying mechanisms of Neat1-BTK interaction were further portrayed. For potential clinical application, the microparticles are developed for effective si-Neat1 delivery, leading to a dramatically enhanced effect for the treatment of osteolysis, which might be a novel strategy to extend the life of the implant.
[Display omitted]</description><identifier>ISSN: 1742-7061</identifier><identifier>EISSN: 1878-7568</identifier><identifier>DOI: 10.1016/j.actbio.2022.02.007</identifier><identifier>PMID: 35151924</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Animals ; Artificial joints ; Aseptic loosening ; Biomedical materials ; Bone implants ; Bone marrow ; Bruton's tyrosine kinase ; Inflammation ; Inflammation - metabolism ; Inflammatory response ; Joint Prosthesis - adverse effects ; Kinases ; KLF4 protein ; lncRNAs ; Macrophage inflammatory response ; Macrophages ; Macrophages - metabolism ; Mice ; Microparticles ; miRNA ; NF-kappa B - metabolism ; NF-κB protein ; NLR Family, Pyrin Domain-Containing 3 Protein ; Non-coding RNA ; Osteolysis ; Osteolysis - chemically induced ; Osteolysis - drug therapy ; Particulate matter ; Polylactide-co-glycolide ; Post-transcription ; Prostheses ; Protein-tyrosine kinase ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Therapeutic targets ; Titanium ; Titanium - adverse effects ; Tyrosine ; Wear particles</subject><ispartof>Acta biomaterialia, 2022-04, Vol.142, p.345-360</ispartof><rights>2022</rights><rights>Copyright © 2022. Published by Elsevier Ltd.</rights><rights>Copyright Elsevier BV Apr 1, 2022</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-8d3671b7863fc7abd8c9339dd76272d51c531d9f6c9e1c365d6cf99e176fc2653</citedby><cites>FETCH-LOGICAL-c390t-8d3671b7863fc7abd8c9339dd76272d51c531d9f6c9e1c365d6cf99e176fc2653</cites><orcidid>0000-0002-7781-1667 ; 0000-0002-0431-4213</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1742706122000848$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35151924$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lin, Sipeng</creatorcontrib><creatorcontrib>Wen, Zhenkang</creatorcontrib><creatorcontrib>Li, Shixun</creatorcontrib><creatorcontrib>Chen, Zhong</creatorcontrib><creatorcontrib>Li, Changchuan</creatorcontrib><creatorcontrib>Ouyang, Zhuji</creatorcontrib><creatorcontrib>Lin, Chuangxin</creatorcontrib><creatorcontrib>Kuang, Manyuan</creatorcontrib><creatorcontrib>Xue, Chunyu</creatorcontrib><creatorcontrib>Ding, Yue</creatorcontrib><title>LncRNA Neat1 promotes the macrophage inflammatory response and acts as a therapeutic target in titanium particle-induced osteolysis</title><title>Acta biomaterialia</title><addtitle>Acta Biomater</addtitle><description>Aseptic loosening (AL), secondary to particle-caused periprosthetic osteolysis, is one of the main reasons of artificial joint failure. Suppressing the macrophage inflammatory response caused by wear particles extends the life of prosthesis, and the long noncoding RNAs (lncRNAs) may play a predominant part in it. Here, titanium particles’ (TiPs’) stimulation increases both the cytoplasmic and nuclear levels of lncRNA Neat1 in bone marrow derived macrophages (BMDMs), which further induces the inflammatory response. Mechanically, Neat1 facilitates Bruton's tyrosine kinase (BTK) transcription by reducing the transcriptional factor KLF4, which further activates the NF-κB pathway, NLRP3 inflammation, and M1 polarization in BMDMs. Cytoplasmic Neat1 also works as an miRNA sponge in miR-188–5p-regulated BTK expression in the post-transcriptional stage. In vivo, Neat1 downregulation can reduce the TiP-induced pro-inflammatory factors and reverse the osteolysis induced by BTK overexpression. In addition, the PLGA-based microparticles loaded with si-Neat1 are developed for the treatment of the mouse calvarial osteolysis model via local injection, presenting satisfactory anti-osteolysis efficacy. These findings indicate that Neat1 is a key regulator of AL.
Due to released particles, aseptic loosening (AL) is the most common reason for prosthesis failure and surgical revision and represents a substantial economic burden worldwide. Herein, we reported that lncRNA Neat1 is a key regulator in regulating wear particles-induced osteolysis by activating NF-κB pathway, NLRP3 inflammation and M1 polarization via BTK, and the underlying mechanisms of Neat1-BTK interaction were further portrayed. For potential clinical application, the microparticles are developed for effective si-Neat1 delivery, leading to a dramatically enhanced effect for the treatment of osteolysis, which might be a novel strategy to extend the life of the implant.
[Display omitted]</description><subject>Animals</subject><subject>Artificial joints</subject><subject>Aseptic loosening</subject><subject>Biomedical materials</subject><subject>Bone implants</subject><subject>Bone marrow</subject><subject>Bruton's tyrosine kinase</subject><subject>Inflammation</subject><subject>Inflammation - metabolism</subject><subject>Inflammatory response</subject><subject>Joint Prosthesis - adverse effects</subject><subject>Kinases</subject><subject>KLF4 protein</subject><subject>lncRNAs</subject><subject>Macrophage inflammatory response</subject><subject>Macrophages</subject><subject>Macrophages - metabolism</subject><subject>Mice</subject><subject>Microparticles</subject><subject>miRNA</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein</subject><subject>Non-coding RNA</subject><subject>Osteolysis</subject><subject>Osteolysis - chemically induced</subject><subject>Osteolysis - drug therapy</subject><subject>Particulate matter</subject><subject>Polylactide-co-glycolide</subject><subject>Post-transcription</subject><subject>Prostheses</subject><subject>Protein-tyrosine kinase</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Therapeutic targets</subject><subject>Titanium</subject><subject>Titanium - adverse effects</subject><subject>Tyrosine</subject><subject>Wear particles</subject><issn>1742-7061</issn><issn>1878-7568</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUuLFDEUhYMozjj6D0QCbtxUTx6VR22EYfAFzQwMug7p5NZMmqqkTFJCr-ePm6ZHFy6EC7mQ79zcnIPQW0o2lFB5ud9YV3chbRhhbENaEfUMnVOtdKeE1M9br3rWKSLpGXpVyp4QrinTL9EZF1TQgfXn6HEb3d3NFb4BWylecppThYLrA-DZupyWB3sPOMRxsvNsa8oHnKEsKRbANnrcdijYtjpKsl1grcHhavM91CbDNVQbwzrjxeZ2M0EXol8deJxKhTQdSiiv0YvRTgXePJ0X6MfnT9-vv3bb2y_frq-2neMDqZ32XCq6U1ry0Sm789oNnA_eK8kU84I6wakfRukGoI5L4aUbh9YrOTomBb9AH05z2zd_rlCqmUNxME02QlqLYZJpOfRUH9H3_6D7tObYtmuUEFT2jOpG9SeqGVVKhtEsOcw2Hwwl5hiS2ZtTSOYYkiGtiGqyd0_D190M_q_oTyoN-HgCoLnxK0A2xQWIzbWQwVXjU_j_C78BjpGmNA</recordid><startdate>20220401</startdate><enddate>20220401</enddate><creator>Lin, Sipeng</creator><creator>Wen, Zhenkang</creator><creator>Li, Shixun</creator><creator>Chen, Zhong</creator><creator>Li, Changchuan</creator><creator>Ouyang, Zhuji</creator><creator>Lin, Chuangxin</creator><creator>Kuang, Manyuan</creator><creator>Xue, Chunyu</creator><creator>Ding, Yue</creator><general>Elsevier Ltd</general><general>Elsevier BV</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>7QF</scope><scope>7QO</scope><scope>7QQ</scope><scope>7SC</scope><scope>7SE</scope><scope>7SP</scope><scope>7SR</scope><scope>7T7</scope><scope>7TA</scope><scope>7TB</scope><scope>7U5</scope><scope>8BQ</scope><scope>8FD</scope><scope>C1K</scope><scope>F28</scope><scope>FR3</scope><scope>H8D</scope><scope>H8G</scope><scope>JG9</scope><scope>JQ2</scope><scope>KR7</scope><scope>L7M</scope><scope>L~C</scope><scope>L~D</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-7781-1667</orcidid><orcidid>https://orcid.org/0000-0002-0431-4213</orcidid></search><sort><creationdate>20220401</creationdate><title>LncRNA Neat1 promotes the macrophage inflammatory response and acts as a therapeutic target in titanium particle-induced osteolysis</title><author>Lin, Sipeng ; Wen, Zhenkang ; Li, Shixun ; Chen, Zhong ; Li, Changchuan ; Ouyang, Zhuji ; Lin, Chuangxin ; Kuang, Manyuan ; Xue, Chunyu ; Ding, Yue</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-8d3671b7863fc7abd8c9339dd76272d51c531d9f6c9e1c365d6cf99e176fc2653</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Animals</topic><topic>Artificial joints</topic><topic>Aseptic loosening</topic><topic>Biomedical materials</topic><topic>Bone implants</topic><topic>Bone marrow</topic><topic>Bruton's tyrosine kinase</topic><topic>Inflammation</topic><topic>Inflammation - metabolism</topic><topic>Inflammatory response</topic><topic>Joint Prosthesis - adverse effects</topic><topic>Kinases</topic><topic>KLF4 protein</topic><topic>lncRNAs</topic><topic>Macrophage inflammatory response</topic><topic>Macrophages</topic><topic>Macrophages - metabolism</topic><topic>Mice</topic><topic>Microparticles</topic><topic>miRNA</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein</topic><topic>Non-coding RNA</topic><topic>Osteolysis</topic><topic>Osteolysis - chemically induced</topic><topic>Osteolysis - drug therapy</topic><topic>Particulate matter</topic><topic>Polylactide-co-glycolide</topic><topic>Post-transcription</topic><topic>Prostheses</topic><topic>Protein-tyrosine kinase</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Therapeutic targets</topic><topic>Titanium</topic><topic>Titanium - adverse effects</topic><topic>Tyrosine</topic><topic>Wear particles</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lin, Sipeng</creatorcontrib><creatorcontrib>Wen, Zhenkang</creatorcontrib><creatorcontrib>Li, Shixun</creatorcontrib><creatorcontrib>Chen, Zhong</creatorcontrib><creatorcontrib>Li, Changchuan</creatorcontrib><creatorcontrib>Ouyang, Zhuji</creatorcontrib><creatorcontrib>Lin, Chuangxin</creatorcontrib><creatorcontrib>Kuang, Manyuan</creatorcontrib><creatorcontrib>Xue, Chunyu</creatorcontrib><creatorcontrib>Ding, Yue</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Aluminium Industry Abstracts</collection><collection>Biotechnology Research Abstracts</collection><collection>Ceramic Abstracts</collection><collection>Computer and Information Systems Abstracts</collection><collection>Corrosion Abstracts</collection><collection>Electronics & Communications Abstracts</collection><collection>Engineered Materials Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Materials Business File</collection><collection>Mechanical & Transportation Engineering Abstracts</collection><collection>Solid State and Superconductivity Abstracts</collection><collection>METADEX</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ANTE: Abstracts in New Technology & Engineering</collection><collection>Engineering Research Database</collection><collection>Aerospace Database</collection><collection>Copper Technical Reference Library</collection><collection>Materials Research Database</collection><collection>ProQuest Computer Science Collection</collection><collection>Civil Engineering Abstracts</collection><collection>Advanced Technologies Database with Aerospace</collection><collection>Computer and Information Systems Abstracts Academic</collection><collection>Computer and Information Systems Abstracts Professional</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Acta biomaterialia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lin, Sipeng</au><au>Wen, Zhenkang</au><au>Li, Shixun</au><au>Chen, Zhong</au><au>Li, Changchuan</au><au>Ouyang, Zhuji</au><au>Lin, Chuangxin</au><au>Kuang, Manyuan</au><au>Xue, Chunyu</au><au>Ding, Yue</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>LncRNA Neat1 promotes the macrophage inflammatory response and acts as a therapeutic target in titanium particle-induced osteolysis</atitle><jtitle>Acta biomaterialia</jtitle><addtitle>Acta Biomater</addtitle><date>2022-04-01</date><risdate>2022</risdate><volume>142</volume><spage>345</spage><epage>360</epage><pages>345-360</pages><issn>1742-7061</issn><eissn>1878-7568</eissn><abstract>Aseptic loosening (AL), secondary to particle-caused periprosthetic osteolysis, is one of the main reasons of artificial joint failure. Suppressing the macrophage inflammatory response caused by wear particles extends the life of prosthesis, and the long noncoding RNAs (lncRNAs) may play a predominant part in it. Here, titanium particles’ (TiPs’) stimulation increases both the cytoplasmic and nuclear levels of lncRNA Neat1 in bone marrow derived macrophages (BMDMs), which further induces the inflammatory response. Mechanically, Neat1 facilitates Bruton's tyrosine kinase (BTK) transcription by reducing the transcriptional factor KLF4, which further activates the NF-κB pathway, NLRP3 inflammation, and M1 polarization in BMDMs. Cytoplasmic Neat1 also works as an miRNA sponge in miR-188–5p-regulated BTK expression in the post-transcriptional stage. In vivo, Neat1 downregulation can reduce the TiP-induced pro-inflammatory factors and reverse the osteolysis induced by BTK overexpression. In addition, the PLGA-based microparticles loaded with si-Neat1 are developed for the treatment of the mouse calvarial osteolysis model via local injection, presenting satisfactory anti-osteolysis efficacy. These findings indicate that Neat1 is a key regulator of AL.
Due to released particles, aseptic loosening (AL) is the most common reason for prosthesis failure and surgical revision and represents a substantial economic burden worldwide. Herein, we reported that lncRNA Neat1 is a key regulator in regulating wear particles-induced osteolysis by activating NF-κB pathway, NLRP3 inflammation and M1 polarization via BTK, and the underlying mechanisms of Neat1-BTK interaction were further portrayed. For potential clinical application, the microparticles are developed for effective si-Neat1 delivery, leading to a dramatically enhanced effect for the treatment of osteolysis, which might be a novel strategy to extend the life of the implant.
[Display omitted]</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>35151924</pmid><doi>10.1016/j.actbio.2022.02.007</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0002-7781-1667</orcidid><orcidid>https://orcid.org/0000-0002-0431-4213</orcidid></addata></record> |
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| subjects | Animals Artificial joints Aseptic loosening Biomedical materials Bone implants Bone marrow Bruton's tyrosine kinase Inflammation Inflammation - metabolism Inflammatory response Joint Prosthesis - adverse effects Kinases KLF4 protein lncRNAs Macrophage inflammatory response Macrophages Macrophages - metabolism Mice Microparticles miRNA NF-kappa B - metabolism NF-κB protein NLR Family, Pyrin Domain-Containing 3 Protein Non-coding RNA Osteolysis Osteolysis - chemically induced Osteolysis - drug therapy Particulate matter Polylactide-co-glycolide Post-transcription Prostheses Protein-tyrosine kinase RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Therapeutic targets Titanium Titanium - adverse effects Tyrosine Wear particles |
| title | LncRNA Neat1 promotes the macrophage inflammatory response and acts as a therapeutic target in titanium particle-induced osteolysis |
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