Modulation of the K/BxN arthritis mouse model and the effector functions of human fibroblast‐like synoviocytes by liver X receptors
The role of liver X receptors (LXR) in rheumatoid arthritis (RA) remains controversial. We studied the effect of LXR agonists on fibroblast‐like synoviocytes (FLS) from RA patients and the K/BxN arthritis model in LXRα and β double‐deficient (Nr1h2/3−/−) mice. Two synthetic LXR agonists, GW3965 and...
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| creator | Domínguez‐Luis, María Jesús Castro‐Hernández, Javier Santos‐Concepción, Sergio Díaz‐Martín, Ana Arce‐Franco, Mayte Pérez‐González, Natán Díaz, Mercedes Castrillo, Antonio Salido, Eduardo Machado, José David Gumá, Mónica Corr, Maripat Díaz‐González, Federico |
| description | The role of liver X receptors (LXR) in rheumatoid arthritis (RA) remains controversial. We studied the effect of LXR agonists on fibroblast‐like synoviocytes (FLS) from RA patients and the K/BxN arthritis model in LXRα and β double‐deficient (Nr1h2/3−/−) mice. Two synthetic LXR agonists, GW3965 and T0901317, were used to activate LXRs and investigate their effects on cell growth, proliferation and matrix metalloproteinases, and chemokine production in cultured FLS from RA patients. The murine model K/BxN serum transfer of inflammatory arthritis in Nr1h2/3−/− animals was used to investigate the role of LXRs on joint inflammation in vivo. LXR agonists inhibited the FLS proliferative capacity in response to TNF, the chemokine‐induced migration, the collagenase activity in FLS supernatant and FLS CXCL12 production. In the K/BxN mouse model, Nr1h2/3−/− animals showed aggravated arthritis, histological inflammation, and joint destruction, as well as an increase in synovial metalloproteases and expression of proinflammatory mediators such as IL‐1β and CCL2 in joints compared with wild type animals. Taken together, these data underscore the importance of LXRs in modulating the joint inflammatory response and highlight them as potential therapeutic targets in RA.
In the K/BxN arthritis mouse model, Nr1h2/3−/− animals showed exacerbated arthritis, histologic inflammation and joint destruction, and increased synovial metalloproteases, IL‐1β and CCL2 in joints compared with wild‐type animals. In FLS from RA patients, LXR agonists inhibited cell proliferation and collagenase activity in response to TNF, chemokine‐induced migration, and CXCL12 production. |
| doi_str_mv | 10.1002/eji.202451136 |
| format | Article |
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In the K/BxN arthritis mouse model, Nr1h2/3−/− animals showed exacerbated arthritis, histologic inflammation and joint destruction, and increased synovial metalloproteases, IL‐1β and CCL2 in joints compared with wild‐type animals. In FLS from RA patients, LXR agonists inhibited cell proliferation and collagenase activity in response to TNF, chemokine‐induced migration, and CXCL12 production.</description><identifier>ISSN: 0014-2980</identifier><identifier>ISSN: 1521-4141</identifier><identifier>EISSN: 1521-4141</identifier><identifier>DOI: 10.1002/eji.202451136</identifier><identifier>PMID: 39148175</identifier><language>eng</language><publisher>Germany: Wiley Subscription Services, Inc</publisher><subject>Agonists ; Animal models ; Animals ; Arthritis ; Arthritis, Experimental - immunology ; Arthritis, Experimental - metabolism ; Arthritis, Experimental - pathology ; Arthritis, Rheumatoid - immunology ; Arthritis, Rheumatoid - metabolism ; Arthritis, Rheumatoid - pathology ; Benzylamines - pharmacology ; Cell Proliferation ; Cells, Cultured ; Chemokines ; Collagenase ; CXCL12 protein ; Disease Models, Animal ; Female ; Fibroblasts ; Fibroblasts - metabolism ; Fibroblast‐like synoviocytes ; Humans ; Inflammation ; Joint diseases ; K/BxN ; Liver X receptors ; Liver X Receptors - genetics ; Liver X Receptors - metabolism ; LXRs ; Male ; Matrix metalloproteinase ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Monocyte chemoattractant protein 1 ; Rheumatoid arthritis ; Synoviocytes ; Synoviocytes - metabolism ; Synoviocytes - pathology ; Therapeutic targets</subject><ispartof>European journal of immunology, 2024-11, Vol.54 (11), p.e2451136-n/a</ispartof><rights>2024 The Author(s). published by Wiley‐VCH GmbH.</rights><rights>2024 The Author(s). European Journal of Immunology published by Wiley‐VCH GmbH.</rights><rights>2024. This article is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). 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><cites>FETCH-LOGICAL-c2899-d11bac89faf49bb3956e9a6ceb5fc8235811190b27bc87625d09ffe6af9719cb3</cites><orcidid>0000-0002-4139-9295</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%2Feji.202451136$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Feji.202451136$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39148175$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Domínguez‐Luis, María Jesús</creatorcontrib><creatorcontrib>Castro‐Hernández, Javier</creatorcontrib><creatorcontrib>Santos‐Concepción, Sergio</creatorcontrib><creatorcontrib>Díaz‐Martín, Ana</creatorcontrib><creatorcontrib>Arce‐Franco, Mayte</creatorcontrib><creatorcontrib>Pérez‐González, Natán</creatorcontrib><creatorcontrib>Díaz, Mercedes</creatorcontrib><creatorcontrib>Castrillo, Antonio</creatorcontrib><creatorcontrib>Salido, Eduardo</creatorcontrib><creatorcontrib>Machado, José David</creatorcontrib><creatorcontrib>Gumá, Mónica</creatorcontrib><creatorcontrib>Corr, Maripat</creatorcontrib><creatorcontrib>Díaz‐González, Federico</creatorcontrib><title>Modulation of the K/BxN arthritis mouse model and the effector functions of human fibroblast‐like synoviocytes by liver X receptors</title><title>European journal of immunology</title><addtitle>Eur J Immunol</addtitle><description>The role of liver X receptors (LXR) in rheumatoid arthritis (RA) remains controversial. We studied the effect of LXR agonists on fibroblast‐like synoviocytes (FLS) from RA patients and the K/BxN arthritis model in LXRα and β double‐deficient (Nr1h2/3−/−) mice. Two synthetic LXR agonists, GW3965 and T0901317, were used to activate LXRs and investigate their effects on cell growth, proliferation and matrix metalloproteinases, and chemokine production in cultured FLS from RA patients. The murine model K/BxN serum transfer of inflammatory arthritis in Nr1h2/3−/− animals was used to investigate the role of LXRs on joint inflammation in vivo. LXR agonists inhibited the FLS proliferative capacity in response to TNF, the chemokine‐induced migration, the collagenase activity in FLS supernatant and FLS CXCL12 production. In the K/BxN mouse model, Nr1h2/3−/− animals showed aggravated arthritis, histological inflammation, and joint destruction, as well as an increase in synovial metalloproteases and expression of proinflammatory mediators such as IL‐1β and CCL2 in joints compared with wild type animals. Taken together, these data underscore the importance of LXRs in modulating the joint inflammatory response and highlight them as potential therapeutic targets in RA.
In the K/BxN arthritis mouse model, Nr1h2/3−/− animals showed exacerbated arthritis, histologic inflammation and joint destruction, and increased synovial metalloproteases, IL‐1β and CCL2 in joints compared with wild‐type animals. In FLS from RA patients, LXR agonists inhibited cell proliferation and collagenase activity in response to TNF, chemokine‐induced migration, and CXCL12 production.</description><subject>Agonists</subject><subject>Animal models</subject><subject>Animals</subject><subject>Arthritis</subject><subject>Arthritis, Experimental - immunology</subject><subject>Arthritis, Experimental - metabolism</subject><subject>Arthritis, Experimental - pathology</subject><subject>Arthritis, Rheumatoid - immunology</subject><subject>Arthritis, Rheumatoid - metabolism</subject><subject>Arthritis, Rheumatoid - pathology</subject><subject>Benzylamines - pharmacology</subject><subject>Cell Proliferation</subject><subject>Cells, Cultured</subject><subject>Chemokines</subject><subject>Collagenase</subject><subject>CXCL12 protein</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Fibroblasts</subject><subject>Fibroblasts - metabolism</subject><subject>Fibroblast‐like synoviocytes</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Joint diseases</subject><subject>K/BxN</subject><subject>Liver X receptors</subject><subject>Liver X Receptors - genetics</subject><subject>Liver X Receptors - metabolism</subject><subject>LXRs</subject><subject>Male</subject><subject>Matrix metalloproteinase</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Rheumatoid arthritis</subject><subject>Synoviocytes</subject><subject>Synoviocytes - metabolism</subject><subject>Synoviocytes - pathology</subject><subject>Therapeutic targets</subject><issn>0014-2980</issn><issn>1521-4141</issn><issn>1521-4141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><recordid>eNp90TFv1DAUB3ALgehRGFmRJZYuaf2cOGePUBUoFFhAYots51nnw4kPOylkY2HnM_JJ8HGlAwOLvfzeX8_-E_IY2Ckwxs9w6085440AqNs7ZAWCQ9VAA3fJijFoKq4kOyIPct4yxlQr1H1yVCtoJKzFivx4G_s56MnHkUZHpw3SN2fPv72jOk2b5Cef6RDnjOXsMVA99n8MOod2iom6ebT74byf3syDHqnzJkUTdJ5-ff8Z_GekeRnjtY92mTBTs9DgrzHRTzShxV1JyQ_JPadDxkc39zH5-OLiw_mr6ur9y8vzZ1eV5VKpqgcw2krltGuUMbUSLSrdWjTCWclrIQFAMcPXxsp1y0XPVFm01U6tQVlTH5OTQ-4uxS8z5qkbfLYYgh6xvLKrmaqFarhsC336D93GOY1lu64GLsrXtlwWVR2UTTHnhK7bJT_otHTAun0_Xemnu-2n-Cc3qbMZsL_VfwspgB_AVx9w-X9ad_H6Ukiu6t9MJp0-</recordid><startdate>202411</startdate><enddate>202411</enddate><creator>Domínguez‐Luis, María Jesús</creator><creator>Castro‐Hernández, Javier</creator><creator>Santos‐Concepción, Sergio</creator><creator>Díaz‐Martín, Ana</creator><creator>Arce‐Franco, Mayte</creator><creator>Pérez‐González, Natán</creator><creator>Díaz, Mercedes</creator><creator>Castrillo, Antonio</creator><creator>Salido, Eduardo</creator><creator>Machado, José David</creator><creator>Gumá, Mónica</creator><creator>Corr, Maripat</creator><creator>Díaz‐González, Federico</creator><general>Wiley Subscription Services, Inc</general><scope>24P</scope><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>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4139-9295</orcidid></search><sort><creationdate>202411</creationdate><title>Modulation of the K/BxN arthritis mouse model and the effector functions of human fibroblast‐like synoviocytes by liver X receptors</title><author>Domínguez‐Luis, María Jesús ; Castro‐Hernández, Javier ; Santos‐Concepción, Sergio ; Díaz‐Martín, Ana ; Arce‐Franco, Mayte ; Pérez‐González, Natán ; Díaz, Mercedes ; Castrillo, Antonio ; Salido, Eduardo ; Machado, José David ; Gumá, Mónica ; Corr, Maripat ; Díaz‐González, Federico</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2899-d11bac89faf49bb3956e9a6ceb5fc8235811190b27bc87625d09ffe6af9719cb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Agonists</topic><topic>Animal models</topic><topic>Animals</topic><topic>Arthritis</topic><topic>Arthritis, Experimental - immunology</topic><topic>Arthritis, Experimental - metabolism</topic><topic>Arthritis, Experimental - pathology</topic><topic>Arthritis, Rheumatoid - immunology</topic><topic>Arthritis, Rheumatoid - metabolism</topic><topic>Arthritis, Rheumatoid - pathology</topic><topic>Benzylamines - pharmacology</topic><topic>Cell Proliferation</topic><topic>Cells, Cultured</topic><topic>Chemokines</topic><topic>Collagenase</topic><topic>CXCL12 protein</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Fibroblasts</topic><topic>Fibroblasts - metabolism</topic><topic>Fibroblast‐like synoviocytes</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Joint diseases</topic><topic>K/BxN</topic><topic>Liver X receptors</topic><topic>Liver X Receptors - genetics</topic><topic>Liver X Receptors - metabolism</topic><topic>LXRs</topic><topic>Male</topic><topic>Matrix metalloproteinase</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Rheumatoid arthritis</topic><topic>Synoviocytes</topic><topic>Synoviocytes - metabolism</topic><topic>Synoviocytes - pathology</topic><topic>Therapeutic targets</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Domínguez‐Luis, María Jesús</creatorcontrib><creatorcontrib>Castro‐Hernández, Javier</creatorcontrib><creatorcontrib>Santos‐Concepción, Sergio</creatorcontrib><creatorcontrib>Díaz‐Martín, Ana</creatorcontrib><creatorcontrib>Arce‐Franco, Mayte</creatorcontrib><creatorcontrib>Pérez‐González, Natán</creatorcontrib><creatorcontrib>Díaz, Mercedes</creatorcontrib><creatorcontrib>Castrillo, Antonio</creatorcontrib><creatorcontrib>Salido, Eduardo</creatorcontrib><creatorcontrib>Machado, José David</creatorcontrib><creatorcontrib>Gumá, Mónica</creatorcontrib><creatorcontrib>Corr, Maripat</creatorcontrib><creatorcontrib>Díaz‐González, Federico</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Domínguez‐Luis, María Jesús</au><au>Castro‐Hernández, Javier</au><au>Santos‐Concepción, Sergio</au><au>Díaz‐Martín, Ana</au><au>Arce‐Franco, Mayte</au><au>Pérez‐González, Natán</au><au>Díaz, Mercedes</au><au>Castrillo, Antonio</au><au>Salido, Eduardo</au><au>Machado, José David</au><au>Gumá, Mónica</au><au>Corr, Maripat</au><au>Díaz‐González, Federico</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modulation of the K/BxN arthritis mouse model and the effector functions of human fibroblast‐like synoviocytes by liver X receptors</atitle><jtitle>European journal of immunology</jtitle><addtitle>Eur J Immunol</addtitle><date>2024-11</date><risdate>2024</risdate><volume>54</volume><issue>11</issue><spage>e2451136</spage><epage>n/a</epage><pages>e2451136-n/a</pages><issn>0014-2980</issn><issn>1521-4141</issn><eissn>1521-4141</eissn><abstract>The role of liver X receptors (LXR) in rheumatoid arthritis (RA) remains controversial. We studied the effect of LXR agonists on fibroblast‐like synoviocytes (FLS) from RA patients and the K/BxN arthritis model in LXRα and β double‐deficient (Nr1h2/3−/−) mice. Two synthetic LXR agonists, GW3965 and T0901317, were used to activate LXRs and investigate their effects on cell growth, proliferation and matrix metalloproteinases, and chemokine production in cultured FLS from RA patients. The murine model K/BxN serum transfer of inflammatory arthritis in Nr1h2/3−/− animals was used to investigate the role of LXRs on joint inflammation in vivo. LXR agonists inhibited the FLS proliferative capacity in response to TNF, the chemokine‐induced migration, the collagenase activity in FLS supernatant and FLS CXCL12 production. In the K/BxN mouse model, Nr1h2/3−/− animals showed aggravated arthritis, histological inflammation, and joint destruction, as well as an increase in synovial metalloproteases and expression of proinflammatory mediators such as IL‐1β and CCL2 in joints compared with wild type animals. Taken together, these data underscore the importance of LXRs in modulating the joint inflammatory response and highlight them as potential therapeutic targets in RA.
In the K/BxN arthritis mouse model, Nr1h2/3−/− animals showed exacerbated arthritis, histologic inflammation and joint destruction, and increased synovial metalloproteases, IL‐1β and CCL2 in joints compared with wild‐type animals. In FLS from RA patients, LXR agonists inhibited cell proliferation and collagenase activity in response to TNF, chemokine‐induced migration, and CXCL12 production.</abstract><cop>Germany</cop><pub>Wiley Subscription Services, Inc</pub><pmid>39148175</pmid><doi>10.1002/eji.202451136</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-4139-9295</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Agonists Animal models Animals Arthritis Arthritis, Experimental - immunology Arthritis, Experimental - metabolism Arthritis, Experimental - pathology Arthritis, Rheumatoid - immunology Arthritis, Rheumatoid - metabolism Arthritis, Rheumatoid - pathology Benzylamines - pharmacology Cell Proliferation Cells, Cultured Chemokines Collagenase CXCL12 protein Disease Models, Animal Female Fibroblasts Fibroblasts - metabolism Fibroblast‐like synoviocytes Humans Inflammation Joint diseases K/BxN Liver X receptors Liver X Receptors - genetics Liver X Receptors - metabolism LXRs Male Matrix metalloproteinase Mice Mice, Inbred C57BL Mice, Knockout Monocyte chemoattractant protein 1 Rheumatoid arthritis Synoviocytes Synoviocytes - metabolism Synoviocytes - pathology Therapeutic targets |
| title | Modulation of the K/BxN arthritis mouse model and the effector functions of human fibroblast‐like synoviocytes by liver X receptors |
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