Exosomal Osteoclast-Derived miRNA in Rheumatoid Arthritis: From Their Pathogenesis in Bone Erosion to New Therapeutic Approaches
Rheumatoid arthritis (RA) is an autoimmune disease that causes inflammation, pain, and ultimately, bone erosion of the joints. The causes of this disease are multifactorial, including genetic factors, such as the presence of the human leukocyte antigen (HLA)-DRB1*04 variant, alterations in the micro...
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| Veröffentlicht in: | International journal of molecular sciences 2024-02, Vol.25 (3), p.1506 |
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| creator | Pascual-García, Sandra Martínez-Peinado, Pascual Pujalte-Satorre, Carolina Navarro-Sempere, Alicia Esteve-Girbés, Jorge López-Jaén, Ana B Javaloyes-Antón, Juan Cobo-Velacoracho, Raúl Navarro-Blasco, Francisco J Sempere-Ortells, José M |
| description | Rheumatoid arthritis (RA) is an autoimmune disease that causes inflammation, pain, and ultimately, bone erosion of the joints. The causes of this disease are multifactorial, including genetic factors, such as the presence of the human leukocyte antigen (HLA)-DRB1*04 variant, alterations in the microbiota, or immune factors including increased cytotoxic T lymphocytes (CTLs), neutrophils, or elevated M1 macrophages which, taken together, produce high levels of pro-inflammatory cytokines. In this review, we focused on the function exerted by osteoclasts on osteoblasts and other osteoclasts by means of the release of exosomal microRNAs (miRNAs). Based on a thorough revision, we classified these molecules into three categories according to their function: osteoclast inhibitors (miR-23a, miR-29b, and miR-214), osteoblast inhibitors (miR-22-3p, miR-26a, miR-27a, miR-29a, miR-125b, and miR-146a), and osteoblast enhancers (miR-20a, miR-34a, miR-96, miR-106a, miR-142, miR-199a, miR-324, and miR-486b). Finally, we analyzed potential therapeutic targets of these exosomal miRNAs, such as the use of antagomiRs, blockmiRs, agomiRs and competitive endogenous RNAs (ceRNAs), which are already being tested in murine and ex vivo models of RA. These strategies might have an important role in reestablishing the regulation of osteoclast and osteoblast differentiation making progress in the development of personalized medicine. |
| doi_str_mv | 10.3390/ijms25031506 |
| format | Article |
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The causes of this disease are multifactorial, including genetic factors, such as the presence of the human leukocyte antigen (HLA)-DRB1*04 variant, alterations in the microbiota, or immune factors including increased cytotoxic T lymphocytes (CTLs), neutrophils, or elevated M1 macrophages which, taken together, produce high levels of pro-inflammatory cytokines. In this review, we focused on the function exerted by osteoclasts on osteoblasts and other osteoclasts by means of the release of exosomal microRNAs (miRNAs). Based on a thorough revision, we classified these molecules into three categories according to their function: osteoclast inhibitors (miR-23a, miR-29b, and miR-214), osteoblast inhibitors (miR-22-3p, miR-26a, miR-27a, miR-29a, miR-125b, and miR-146a), and osteoblast enhancers (miR-20a, miR-34a, miR-96, miR-106a, miR-142, miR-199a, miR-324, and miR-486b). Finally, we analyzed potential therapeutic targets of these exosomal miRNAs, such as the use of antagomiRs, blockmiRs, agomiRs and competitive endogenous RNAs (ceRNAs), which are already being tested in murine and ex vivo models of RA. These strategies might have an important role in reestablishing the regulation of osteoclast and osteoblast differentiation making progress in the development of personalized medicine.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms25031506</identifier><identifier>PMID: 38338785</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Analysis ; Animals ; Antagomirs ; Arthritis ; Arthritis, Rheumatoid - genetics ; Arthritis, Rheumatoid - pathology ; B cells ; Cartilage ; Cytokines ; Development and progression ; Enzymes ; Epigenetics ; Health aspects ; Histocompatibility antigens ; HLA histocompatibility antigens ; Humans ; Immunity ; Inflammation ; Leukocytes ; Lymphocytes ; Macrophages ; Macrophages - pathology ; Mice ; Microbiota (Symbiotic organisms) ; MicroRNA ; MicroRNAs - genetics ; Neutrophils ; Osteoblasts - pathology ; Osteoclasts - pathology ; Pathogenesis ; Proteins ; Rheumatoid arthritis ; T cells ; Tumor necrosis factor-TNF</subject><ispartof>International journal of molecular sciences, 2024-02, Vol.25 (3), p.1506</ispartof><rights>COPYRIGHT 2024 MDPI AG</rights><rights>2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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-c424t-ff8b0560a11c7b4ca0b7bee798e8862b50d70abcdab3fdb5a125dab1855d2283</citedby><cites>FETCH-LOGICAL-c424t-ff8b0560a11c7b4ca0b7bee798e8862b50d70abcdab3fdb5a125dab1855d2283</cites><orcidid>0000-0002-0536-1185 ; 0000-0003-4370-5468</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27902,27903</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38338785$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pascual-García, Sandra</creatorcontrib><creatorcontrib>Martínez-Peinado, Pascual</creatorcontrib><creatorcontrib>Pujalte-Satorre, Carolina</creatorcontrib><creatorcontrib>Navarro-Sempere, Alicia</creatorcontrib><creatorcontrib>Esteve-Girbés, Jorge</creatorcontrib><creatorcontrib>López-Jaén, Ana B</creatorcontrib><creatorcontrib>Javaloyes-Antón, Juan</creatorcontrib><creatorcontrib>Cobo-Velacoracho, Raúl</creatorcontrib><creatorcontrib>Navarro-Blasco, Francisco J</creatorcontrib><creatorcontrib>Sempere-Ortells, José M</creatorcontrib><title>Exosomal Osteoclast-Derived miRNA in Rheumatoid Arthritis: From Their Pathogenesis in Bone Erosion to New Therapeutic Approaches</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Rheumatoid arthritis (RA) is an autoimmune disease that causes inflammation, pain, and ultimately, bone erosion of the joints. The causes of this disease are multifactorial, including genetic factors, such as the presence of the human leukocyte antigen (HLA)-DRB1*04 variant, alterations in the microbiota, or immune factors including increased cytotoxic T lymphocytes (CTLs), neutrophils, or elevated M1 macrophages which, taken together, produce high levels of pro-inflammatory cytokines. In this review, we focused on the function exerted by osteoclasts on osteoblasts and other osteoclasts by means of the release of exosomal microRNAs (miRNAs). Based on a thorough revision, we classified these molecules into three categories according to their function: osteoclast inhibitors (miR-23a, miR-29b, and miR-214), osteoblast inhibitors (miR-22-3p, miR-26a, miR-27a, miR-29a, miR-125b, and miR-146a), and osteoblast enhancers (miR-20a, miR-34a, miR-96, miR-106a, miR-142, miR-199a, miR-324, and miR-486b). Finally, we analyzed potential therapeutic targets of these exosomal miRNAs, such as the use of antagomiRs, blockmiRs, agomiRs and competitive endogenous RNAs (ceRNAs), which are already being tested in murine and ex vivo models of RA. These strategies might have an important role in reestablishing the regulation of osteoclast and osteoblast differentiation making progress in the development of personalized medicine.</description><subject>Analysis</subject><subject>Animals</subject><subject>Antagomirs</subject><subject>Arthritis</subject><subject>Arthritis, Rheumatoid - genetics</subject><subject>Arthritis, Rheumatoid - pathology</subject><subject>B cells</subject><subject>Cartilage</subject><subject>Cytokines</subject><subject>Development and progression</subject><subject>Enzymes</subject><subject>Epigenetics</subject><subject>Health aspects</subject><subject>Histocompatibility antigens</subject><subject>HLA histocompatibility antigens</subject><subject>Humans</subject><subject>Immunity</subject><subject>Inflammation</subject><subject>Leukocytes</subject><subject>Lymphocytes</subject><subject>Macrophages</subject><subject>Macrophages - pathology</subject><subject>Mice</subject><subject>Microbiota (Symbiotic organisms)</subject><subject>MicroRNA</subject><subject>MicroRNAs - genetics</subject><subject>Neutrophils</subject><subject>Osteoblasts - pathology</subject><subject>Osteoclasts - pathology</subject><subject>Pathogenesis</subject><subject>Proteins</subject><subject>Rheumatoid arthritis</subject><subject>T cells</subject><subject>Tumor necrosis factor-TNF</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkc1P3DAQxa0KVD7KrefKEpceCDj2OnG4BVhaJAQI7T2ynQnxKo4X22nLrX96HUFbiqo5zMj6vfHoPYQ-5uSYsYqcmLUNlBOWc1K8Q7v5gtKMkKLcejXvoL0Q1oRQRnn1Hu0wwZgoBd9FP5c_XHBWDvg2RHB6kCFmF-DNN2ixNfc3NTYjvu9hsjI60-Lax96baMIpvvTO4lUPxuM7GXv3ACMEE2bBmRsBL70Lxo04OnwD32fSyw1M0WhcbzbeSd1D-IC2OzkEOHjp-2h1uVydf82ub79cndfXmV7QRcy6TijCCyLzXJdqoSVRpQIoKwFCFFRx0pZEKt1KxbpWcZlTnuZccN5SKtg--vy8Nv37OEGIjTVBwzDIEdwUGlrNHvJKkIQevkHXbvJjOm6mWFVUgvK_1IMcoDFj56KXel7a1KWgpEq2s0Qd_4dK1YI1OpnUmfT-j-DoWaCTecFD12y8sdI_NTlp5ryb13kn_NPLrZOy0P6BfwfMfgGgQqXy</recordid><startdate>20240201</startdate><enddate>20240201</enddate><creator>Pascual-García, Sandra</creator><creator>Martínez-Peinado, Pascual</creator><creator>Pujalte-Satorre, Carolina</creator><creator>Navarro-Sempere, Alicia</creator><creator>Esteve-Girbés, Jorge</creator><creator>López-Jaén, Ana B</creator><creator>Javaloyes-Antón, Juan</creator><creator>Cobo-Velacoracho, Raúl</creator><creator>Navarro-Blasco, Francisco J</creator><creator>Sempere-Ortells, José M</creator><general>MDPI AG</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-0536-1185</orcidid><orcidid>https://orcid.org/0000-0003-4370-5468</orcidid></search><sort><creationdate>20240201</creationdate><title>Exosomal Osteoclast-Derived miRNA in Rheumatoid Arthritis: From Their Pathogenesis in Bone Erosion to New Therapeutic Approaches</title><author>Pascual-García, Sandra ; Martínez-Peinado, Pascual ; Pujalte-Satorre, Carolina ; Navarro-Sempere, Alicia ; Esteve-Girbés, Jorge ; López-Jaén, Ana B ; Javaloyes-Antón, Juan ; Cobo-Velacoracho, Raúl ; Navarro-Blasco, Francisco J ; Sempere-Ortells, José M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c424t-ff8b0560a11c7b4ca0b7bee798e8862b50d70abcdab3fdb5a125dab1855d2283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>Antagomirs</topic><topic>Arthritis</topic><topic>Arthritis, Rheumatoid - 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Academic</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pascual-García, Sandra</au><au>Martínez-Peinado, Pascual</au><au>Pujalte-Satorre, Carolina</au><au>Navarro-Sempere, Alicia</au><au>Esteve-Girbés, Jorge</au><au>López-Jaén, Ana B</au><au>Javaloyes-Antón, Juan</au><au>Cobo-Velacoracho, Raúl</au><au>Navarro-Blasco, Francisco J</au><au>Sempere-Ortells, José M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Exosomal Osteoclast-Derived miRNA in Rheumatoid Arthritis: From Their Pathogenesis in Bone Erosion to New Therapeutic Approaches</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2024-02-01</date><risdate>2024</risdate><volume>25</volume><issue>3</issue><spage>1506</spage><pages>1506-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Rheumatoid arthritis (RA) is an autoimmune disease that causes inflammation, pain, and ultimately, bone erosion of the joints. The causes of this disease are multifactorial, including genetic factors, such as the presence of the human leukocyte antigen (HLA)-DRB1*04 variant, alterations in the microbiota, or immune factors including increased cytotoxic T lymphocytes (CTLs), neutrophils, or elevated M1 macrophages which, taken together, produce high levels of pro-inflammatory cytokines. In this review, we focused on the function exerted by osteoclasts on osteoblasts and other osteoclasts by means of the release of exosomal microRNAs (miRNAs). Based on a thorough revision, we classified these molecules into three categories according to their function: osteoclast inhibitors (miR-23a, miR-29b, and miR-214), osteoblast inhibitors (miR-22-3p, miR-26a, miR-27a, miR-29a, miR-125b, and miR-146a), and osteoblast enhancers (miR-20a, miR-34a, miR-96, miR-106a, miR-142, miR-199a, miR-324, and miR-486b). Finally, we analyzed potential therapeutic targets of these exosomal miRNAs, such as the use of antagomiRs, blockmiRs, agomiRs and competitive endogenous RNAs (ceRNAs), which are already being tested in murine and ex vivo models of RA. These strategies might have an important role in reestablishing the regulation of osteoclast and osteoblast differentiation making progress in the development of personalized medicine.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>38338785</pmid><doi>10.3390/ijms25031506</doi><orcidid>https://orcid.org/0000-0002-0536-1185</orcidid><orcidid>https://orcid.org/0000-0003-4370-5468</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis Animals Antagomirs Arthritis Arthritis, Rheumatoid - genetics Arthritis, Rheumatoid - pathology B cells Cartilage Cytokines Development and progression Enzymes Epigenetics Health aspects Histocompatibility antigens HLA histocompatibility antigens Humans Immunity Inflammation Leukocytes Lymphocytes Macrophages Macrophages - pathology Mice Microbiota (Symbiotic organisms) MicroRNA MicroRNAs - genetics Neutrophils Osteoblasts - pathology Osteoclasts - pathology Pathogenesis Proteins Rheumatoid arthritis T cells Tumor necrosis factor-TNF |
| title | Exosomal Osteoclast-Derived miRNA in Rheumatoid Arthritis: From Their Pathogenesis in Bone Erosion to New Therapeutic Approaches |
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