Study on the expression changes of lncRNA in patients with systemic lupus erythematosus and its correlation with Treg cells
Objectives We initially explored the link between the differentially expressed long non-coding RNAs (lncRNAs) and the number of regulatory T (Treg) cells by detecting the lncRNA expression profiles in patients with systemic lupus erythematosus (SLE), then analyzed the correlation between Treg-relate...
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| Veröffentlicht in: | Clinical rheumatology 2024-03, Vol.43 (3), p.993-1002 |
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| creator | Bu, Yu-jie Cen, Xing Wang, Yi-qi Fan, Ru Zhang, Fen Liu, Yu-qing An, Jia Qiao, Jun Zhang, Sheng-xiao Chen, Jun-wei |
| description | Objectives
We initially explored the link between the differentially expressed long non-coding RNAs (lncRNAs) and the number of regulatory T (Treg) cells by detecting the lncRNA expression profiles in patients with systemic lupus erythematosus (SLE), then analyzed the correlation between Treg-related lncRNAs and the clinical features of SLE patients, predicting the mechanism by which lncRNAs regulate the differentiation and development of Treg cells, and provided new ideas for the treatment of SLE.
Methods
Peripheral blood of 9 active SLE patients were collected and mononuclear cells (PBMCs) were extracted; the lncRNA expression profiles of PBMCs were analyzed by whole transcriptome sequencing. Nine healthy people were used as controls to screen the differentially expressed lncRNAs, to analyze the correlation between lncRNAs and Treg cell number. Pearson test was used to analyze the correlation between lncRNAs and the number of Treg cell, and the correlation between Treg-associated lncRNA and SLEDAI score, ESR, C3, and C4 in SLE patients. The targeted genes of Treg-associated lncRNAs were predicted with miRcode and Targetscan databases and coexpression network.
Results
There were 240 differentially expressed lncRNAs in SLE patients compared with healthy controls, including 134 highly expressed lncRNAs (
p
< 0.05) and 106 lowly expressed lncRNAs (
p
< 0.05). The expression of ANKRD44-AS1 (
r
= 0.7417,
p
= 0.0222), LINC00200 (
r
= 0.6960,
p
= 0.0373), AP001363.2 (
r
= 0.7766,
p
= 0.0138), and LINC02824 (
r
= 0.7893,
p
= 0.0114) were positively correlated with the number of Treg cell, and the expression of AP000640.1 (
r
= − 0.7225,
p
= 0.0279), AC124248.1 (
r
= − 0.7653,
p
= 0.0163), LINC00482 (
r
= − 0.8317,
p
= 0.0054), and MIR503HG (
r
= − 0.7617,
p
< 0.05) were negatively correlated with the number of Treg cell. Among these Treg-associated lncRNAs, the expression of LINC00482 (
r
= − 0.7348,
p
< 0.05) and MIR503 HG (
r
= − 0.7617,
p
< 0.05) were negatively correlated with C3. LINC00200, ANKRD44 - AS1, and AP000640.1 related to Treg cells regulate the expression of signal transducer and activator of transcription 5 (STAT5), phospholipase D1 (PLD1), homeodomain-only protein X (HOPX), and runt-related transcription factor 3 (RUNX3) through competitive binding of miRNA or trans-regulatory mechanism, thereby regulating the differentiation and development of Treg cell.
Conclusions
The lncRNA expression profiles were changed in SLE patients, the differentially |
| doi_str_mv | 10.1007/s10067-023-06844-w |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2917860120</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2928414659</sourcerecordid><originalsourceid>FETCH-LOGICAL-c359t-fc73c365af9821800e5ce9e804653b6fe409b19764d372e62ebf295d71ea4333</originalsourceid><addsrcrecordid>eNqFkU1rFEEQhhtRzJr4BzxIgxcvY_pr-uMYgiZCMGD23vT21GQnzJddPayLf97ebFTwoJcqin7et6p5CXnD2QfOmDnHUrWpmJAV01apaveMrLiSqnJOuedkxYxhleTOnpBXiA-MMWEdf0lOpBW1NJatyI-7vDR7Oo00b4HC9zkBYlfGuA3jPSCdWtqP8euXC9qNdA65gzEj3XV5S3GPGYYu0n6ZF6SQ9sVjCHnCMoWxoV0h45QS9EVXPB9V6wT3NELf4xl50YYe4fVTPyXrTx_Xl9fVze3V58uLmyrK2uWqjUZGqevQOiu4ZQzqCA4sU7qWG92CYm7DndGqkUaAFrBphasbwyEoKeUpeX-0ndP0bQHMfujwcEAYYVrQS16XPbU27r-ocNxYzbhgBX33F_owLWks_yiUsIqX6w6G4kjFNCEmaP2cuiGkvefMH0L0xxB9CdE_huh3RfT2yXrZDND8lvxKrQDyCGB5KimlP7v_YfsTdXWorg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2928414659</pqid></control><display><type>article</type><title>Study on the expression changes of lncRNA in patients with systemic lupus erythematosus and its correlation with Treg cells</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Bu, Yu-jie ; Cen, Xing ; Wang, Yi-qi ; Fan, Ru ; Zhang, Fen ; Liu, Yu-qing ; An, Jia ; Qiao, Jun ; Zhang, Sheng-xiao ; Chen, Jun-wei</creator><creatorcontrib>Bu, Yu-jie ; Cen, Xing ; Wang, Yi-qi ; Fan, Ru ; Zhang, Fen ; Liu, Yu-qing ; An, Jia ; Qiao, Jun ; Zhang, Sheng-xiao ; Chen, Jun-wei</creatorcontrib><description>Objectives
We initially explored the link between the differentially expressed long non-coding RNAs (lncRNAs) and the number of regulatory T (Treg) cells by detecting the lncRNA expression profiles in patients with systemic lupus erythematosus (SLE), then analyzed the correlation between Treg-related lncRNAs and the clinical features of SLE patients, predicting the mechanism by which lncRNAs regulate the differentiation and development of Treg cells, and provided new ideas for the treatment of SLE.
Methods
Peripheral blood of 9 active SLE patients were collected and mononuclear cells (PBMCs) were extracted; the lncRNA expression profiles of PBMCs were analyzed by whole transcriptome sequencing. Nine healthy people were used as controls to screen the differentially expressed lncRNAs, to analyze the correlation between lncRNAs and Treg cell number. Pearson test was used to analyze the correlation between lncRNAs and the number of Treg cell, and the correlation between Treg-associated lncRNA and SLEDAI score, ESR, C3, and C4 in SLE patients. The targeted genes of Treg-associated lncRNAs were predicted with miRcode and Targetscan databases and coexpression network.
Results
There were 240 differentially expressed lncRNAs in SLE patients compared with healthy controls, including 134 highly expressed lncRNAs (
p
< 0.05) and 106 lowly expressed lncRNAs (
p
< 0.05). The expression of ANKRD44-AS1 (
r
= 0.7417,
p
= 0.0222), LINC00200 (
r
= 0.6960,
p
= 0.0373), AP001363.2 (
r
= 0.7766,
p
= 0.0138), and LINC02824 (
r
= 0.7893,
p
= 0.0114) were positively correlated with the number of Treg cell, and the expression of AP000640.1 (
r
= − 0.7225,
p
= 0.0279), AC124248.1 (
r
= − 0.7653,
p
= 0.0163), LINC00482 (
r
= − 0.8317,
p
= 0.0054), and MIR503HG (
r
= − 0.7617,
p
< 0.05) were negatively correlated with the number of Treg cell. Among these Treg-associated lncRNAs, the expression of LINC00482 (
r
= − 0.7348,
p
< 0.05) and MIR503 HG (
r
= − 0.7617,
p
< 0.05) were negatively correlated with C3. LINC00200, ANKRD44 - AS1, and AP000640.1 related to Treg cells regulate the expression of signal transducer and activator of transcription 5 (STAT5), phospholipase D1 (PLD1), homeodomain-only protein X (HOPX), and runt-related transcription factor 3 (RUNX3) through competitive binding of miRNA or trans-regulatory mechanism, thereby regulating the differentiation and development of Treg cell.
Conclusions
The lncRNA expression profiles were changed in SLE patients, the differentially expressed lncRNAs were associated with abnormal number and function of Treg cells in SLE, and Treg-associated lncRNAs were associated with SLE-disease activity, which may affect the expression of STAT5, PLD1, HOPX, RUNX3 and regulate Treg cell function and participate in the pathogenesis and progression of SLE by competitively binding to miRNAs or trans-regulatory mechanism.
Key points
• Systemic lupus erythematosus (SLE) is an autoimmune disease involving multiple organs and systems. lncRNAs may affect Treg cells function by regulating genes expression, which may be an important pathogenesis of SLE.
• This study, taking SLE as an example, preliminarily analyzed the correlation between lncRNA and Treg cells in SLE patients, analyzed the correlation between Treg-related lncRNA and the clinical characteristics of SLE, and speculated that lncRNA could regulate the differentiation and development of Treg cells through competitive combination with miRNA or trans-regulatory mechanisms.
• It is possible to target epigenetic therapy for SLE.</description><identifier>ISSN: 0770-3198</identifier><identifier>EISSN: 1434-9949</identifier><identifier>DOI: 10.1007/s10067-023-06844-w</identifier><identifier>PMID: 38253780</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Autoimmune diseases ; blood ; Cell differentiation ; Cell number ; Epigenetics ; Homeobox ; Humans ; Leukocytes (mononuclear) ; Lupus ; lupus erythematosus ; Lupus Erythematosus, Systemic ; Lymphocytes T ; Medicine ; Medicine & Public Health ; microRNA ; MicroRNAs ; MicroRNAs - genetics ; miRNA ; Non-coding RNA ; Original Article ; Pathogenesis ; Patients ; people ; Peripheral blood ; Phospholipase D1 ; phospholipases ; Protein X ; Rheumatology ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Runx3 protein ; signal transduction ; Stat5 protein ; STAT5 Transcription Factor - metabolism ; Systemic lupus erythematosus ; T-Lymphocytes, Regulatory ; therapeutics ; transactivators ; transcriptome ; Transcriptomes</subject><ispartof>Clinical rheumatology, 2024-03, Vol.43 (3), p.993-1002</ispartof><rights>The Author(s), under exclusive licence to International League of Associations for Rheumatology (ILAR) 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 International League of Associations for Rheumatology (ILAR).</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c359t-fc73c365af9821800e5ce9e804653b6fe409b19764d372e62ebf295d71ea4333</cites><orcidid>0000-0001-5053-9651</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/s10067-023-06844-w$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10067-023-06844-w$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38253780$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bu, Yu-jie</creatorcontrib><creatorcontrib>Cen, Xing</creatorcontrib><creatorcontrib>Wang, Yi-qi</creatorcontrib><creatorcontrib>Fan, Ru</creatorcontrib><creatorcontrib>Zhang, Fen</creatorcontrib><creatorcontrib>Liu, Yu-qing</creatorcontrib><creatorcontrib>An, Jia</creatorcontrib><creatorcontrib>Qiao, Jun</creatorcontrib><creatorcontrib>Zhang, Sheng-xiao</creatorcontrib><creatorcontrib>Chen, Jun-wei</creatorcontrib><title>Study on the expression changes of lncRNA in patients with systemic lupus erythematosus and its correlation with Treg cells</title><title>Clinical rheumatology</title><addtitle>Clin Rheumatol</addtitle><addtitle>Clin Rheumatol</addtitle><description>Objectives
We initially explored the link between the differentially expressed long non-coding RNAs (lncRNAs) and the number of regulatory T (Treg) cells by detecting the lncRNA expression profiles in patients with systemic lupus erythematosus (SLE), then analyzed the correlation between Treg-related lncRNAs and the clinical features of SLE patients, predicting the mechanism by which lncRNAs regulate the differentiation and development of Treg cells, and provided new ideas for the treatment of SLE.
Methods
Peripheral blood of 9 active SLE patients were collected and mononuclear cells (PBMCs) were extracted; the lncRNA expression profiles of PBMCs were analyzed by whole transcriptome sequencing. Nine healthy people were used as controls to screen the differentially expressed lncRNAs, to analyze the correlation between lncRNAs and Treg cell number. Pearson test was used to analyze the correlation between lncRNAs and the number of Treg cell, and the correlation between Treg-associated lncRNA and SLEDAI score, ESR, C3, and C4 in SLE patients. The targeted genes of Treg-associated lncRNAs were predicted with miRcode and Targetscan databases and coexpression network.
Results
There were 240 differentially expressed lncRNAs in SLE patients compared with healthy controls, including 134 highly expressed lncRNAs (
p
< 0.05) and 106 lowly expressed lncRNAs (
p
< 0.05). The expression of ANKRD44-AS1 (
r
= 0.7417,
p
= 0.0222), LINC00200 (
r
= 0.6960,
p
= 0.0373), AP001363.2 (
r
= 0.7766,
p
= 0.0138), and LINC02824 (
r
= 0.7893,
p
= 0.0114) were positively correlated with the number of Treg cell, and the expression of AP000640.1 (
r
= − 0.7225,
p
= 0.0279), AC124248.1 (
r
= − 0.7653,
p
= 0.0163), LINC00482 (
r
= − 0.8317,
p
= 0.0054), and MIR503HG (
r
= − 0.7617,
p
< 0.05) were negatively correlated with the number of Treg cell. Among these Treg-associated lncRNAs, the expression of LINC00482 (
r
= − 0.7348,
p
< 0.05) and MIR503 HG (
r
= − 0.7617,
p
< 0.05) were negatively correlated with C3. LINC00200, ANKRD44 - AS1, and AP000640.1 related to Treg cells regulate the expression of signal transducer and activator of transcription 5 (STAT5), phospholipase D1 (PLD1), homeodomain-only protein X (HOPX), and runt-related transcription factor 3 (RUNX3) through competitive binding of miRNA or trans-regulatory mechanism, thereby regulating the differentiation and development of Treg cell.
Conclusions
The lncRNA expression profiles were changed in SLE patients, the differentially expressed lncRNAs were associated with abnormal number and function of Treg cells in SLE, and Treg-associated lncRNAs were associated with SLE-disease activity, which may affect the expression of STAT5, PLD1, HOPX, RUNX3 and regulate Treg cell function and participate in the pathogenesis and progression of SLE by competitively binding to miRNAs or trans-regulatory mechanism.
Key points
• Systemic lupus erythematosus (SLE) is an autoimmune disease involving multiple organs and systems. lncRNAs may affect Treg cells function by regulating genes expression, which may be an important pathogenesis of SLE.
• This study, taking SLE as an example, preliminarily analyzed the correlation between lncRNA and Treg cells in SLE patients, analyzed the correlation between Treg-related lncRNA and the clinical characteristics of SLE, and speculated that lncRNA could regulate the differentiation and development of Treg cells through competitive combination with miRNA or trans-regulatory mechanisms.
• It is possible to target epigenetic therapy for SLE.</description><subject>Autoimmune diseases</subject><subject>blood</subject><subject>Cell differentiation</subject><subject>Cell number</subject><subject>Epigenetics</subject><subject>Homeobox</subject><subject>Humans</subject><subject>Leukocytes (mononuclear)</subject><subject>Lupus</subject><subject>lupus erythematosus</subject><subject>Lupus Erythematosus, Systemic</subject><subject>Lymphocytes T</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>microRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>miRNA</subject><subject>Non-coding RNA</subject><subject>Original Article</subject><subject>Pathogenesis</subject><subject>Patients</subject><subject>people</subject><subject>Peripheral blood</subject><subject>Phospholipase D1</subject><subject>phospholipases</subject><subject>Protein X</subject><subject>Rheumatology</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Runx3 protein</subject><subject>signal transduction</subject><subject>Stat5 protein</subject><subject>STAT5 Transcription Factor - metabolism</subject><subject>Systemic lupus erythematosus</subject><subject>T-Lymphocytes, Regulatory</subject><subject>therapeutics</subject><subject>transactivators</subject><subject>transcriptome</subject><subject>Transcriptomes</subject><issn>0770-3198</issn><issn>1434-9949</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1rFEEQhhtRzJr4BzxIgxcvY_pr-uMYgiZCMGD23vT21GQnzJddPayLf97ebFTwoJcqin7et6p5CXnD2QfOmDnHUrWpmJAV01apaveMrLiSqnJOuedkxYxhleTOnpBXiA-MMWEdf0lOpBW1NJatyI-7vDR7Oo00b4HC9zkBYlfGuA3jPSCdWtqP8euXC9qNdA65gzEj3XV5S3GPGYYu0n6ZF6SQ9sVjCHnCMoWxoV0h45QS9EVXPB9V6wT3NELf4xl50YYe4fVTPyXrTx_Xl9fVze3V58uLmyrK2uWqjUZGqevQOiu4ZQzqCA4sU7qWG92CYm7DndGqkUaAFrBphasbwyEoKeUpeX-0ndP0bQHMfujwcEAYYVrQS16XPbU27r-ocNxYzbhgBX33F_owLWks_yiUsIqX6w6G4kjFNCEmaP2cuiGkvefMH0L0xxB9CdE_huh3RfT2yXrZDND8lvxKrQDyCGB5KimlP7v_YfsTdXWorg</recordid><startdate>20240301</startdate><enddate>20240301</enddate><creator>Bu, Yu-jie</creator><creator>Cen, Xing</creator><creator>Wang, Yi-qi</creator><creator>Fan, Ru</creator><creator>Zhang, Fen</creator><creator>Liu, Yu-qing</creator><creator>An, Jia</creator><creator>Qiao, Jun</creator><creator>Zhang, Sheng-xiao</creator><creator>Chen, Jun-wei</creator><general>Springer International Publishing</general><general>Springer Nature B.V</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>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><scope>7S9</scope><scope>L.6</scope><orcidid>https://orcid.org/0000-0001-5053-9651</orcidid></search><sort><creationdate>20240301</creationdate><title>Study on the expression changes of lncRNA in patients with systemic lupus erythematosus and its correlation with Treg cells</title><author>Bu, Yu-jie ; Cen, Xing ; Wang, Yi-qi ; Fan, Ru ; Zhang, Fen ; Liu, Yu-qing ; An, Jia ; Qiao, Jun ; Zhang, Sheng-xiao ; Chen, Jun-wei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c359t-fc73c365af9821800e5ce9e804653b6fe409b19764d372e62ebf295d71ea4333</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Autoimmune diseases</topic><topic>blood</topic><topic>Cell differentiation</topic><topic>Cell number</topic><topic>Epigenetics</topic><topic>Homeobox</topic><topic>Humans</topic><topic>Leukocytes (mononuclear)</topic><topic>Lupus</topic><topic>lupus erythematosus</topic><topic>Lupus Erythematosus, Systemic</topic><topic>Lymphocytes T</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>microRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>miRNA</topic><topic>Non-coding RNA</topic><topic>Original Article</topic><topic>Pathogenesis</topic><topic>Patients</topic><topic>people</topic><topic>Peripheral blood</topic><topic>Phospholipase D1</topic><topic>phospholipases</topic><topic>Protein X</topic><topic>Rheumatology</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Runx3 protein</topic><topic>signal transduction</topic><topic>Stat5 protein</topic><topic>STAT5 Transcription Factor - metabolism</topic><topic>Systemic lupus erythematosus</topic><topic>T-Lymphocytes, Regulatory</topic><topic>therapeutics</topic><topic>transactivators</topic><topic>transcriptome</topic><topic>Transcriptomes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bu, Yu-jie</creatorcontrib><creatorcontrib>Cen, Xing</creatorcontrib><creatorcontrib>Wang, Yi-qi</creatorcontrib><creatorcontrib>Fan, Ru</creatorcontrib><creatorcontrib>Zhang, Fen</creatorcontrib><creatorcontrib>Liu, Yu-qing</creatorcontrib><creatorcontrib>An, Jia</creatorcontrib><creatorcontrib>Qiao, Jun</creatorcontrib><creatorcontrib>Zhang, Sheng-xiao</creatorcontrib><creatorcontrib>Chen, Jun-wei</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>Clinical rheumatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bu, Yu-jie</au><au>Cen, Xing</au><au>Wang, Yi-qi</au><au>Fan, Ru</au><au>Zhang, Fen</au><au>Liu, Yu-qing</au><au>An, Jia</au><au>Qiao, Jun</au><au>Zhang, Sheng-xiao</au><au>Chen, Jun-wei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Study on the expression changes of lncRNA in patients with systemic lupus erythematosus and its correlation with Treg cells</atitle><jtitle>Clinical rheumatology</jtitle><stitle>Clin Rheumatol</stitle><addtitle>Clin Rheumatol</addtitle><date>2024-03-01</date><risdate>2024</risdate><volume>43</volume><issue>3</issue><spage>993</spage><epage>1002</epage><pages>993-1002</pages><issn>0770-3198</issn><eissn>1434-9949</eissn><abstract>Objectives
We initially explored the link between the differentially expressed long non-coding RNAs (lncRNAs) and the number of regulatory T (Treg) cells by detecting the lncRNA expression profiles in patients with systemic lupus erythematosus (SLE), then analyzed the correlation between Treg-related lncRNAs and the clinical features of SLE patients, predicting the mechanism by which lncRNAs regulate the differentiation and development of Treg cells, and provided new ideas for the treatment of SLE.
Methods
Peripheral blood of 9 active SLE patients were collected and mononuclear cells (PBMCs) were extracted; the lncRNA expression profiles of PBMCs were analyzed by whole transcriptome sequencing. Nine healthy people were used as controls to screen the differentially expressed lncRNAs, to analyze the correlation between lncRNAs and Treg cell number. Pearson test was used to analyze the correlation between lncRNAs and the number of Treg cell, and the correlation between Treg-associated lncRNA and SLEDAI score, ESR, C3, and C4 in SLE patients. The targeted genes of Treg-associated lncRNAs were predicted with miRcode and Targetscan databases and coexpression network.
Results
There were 240 differentially expressed lncRNAs in SLE patients compared with healthy controls, including 134 highly expressed lncRNAs (
p
< 0.05) and 106 lowly expressed lncRNAs (
p
< 0.05). The expression of ANKRD44-AS1 (
r
= 0.7417,
p
= 0.0222), LINC00200 (
r
= 0.6960,
p
= 0.0373), AP001363.2 (
r
= 0.7766,
p
= 0.0138), and LINC02824 (
r
= 0.7893,
p
= 0.0114) were positively correlated with the number of Treg cell, and the expression of AP000640.1 (
r
= − 0.7225,
p
= 0.0279), AC124248.1 (
r
= − 0.7653,
p
= 0.0163), LINC00482 (
r
= − 0.8317,
p
= 0.0054), and MIR503HG (
r
= − 0.7617,
p
< 0.05) were negatively correlated with the number of Treg cell. Among these Treg-associated lncRNAs, the expression of LINC00482 (
r
= − 0.7348,
p
< 0.05) and MIR503 HG (
r
= − 0.7617,
p
< 0.05) were negatively correlated with C3. LINC00200, ANKRD44 - AS1, and AP000640.1 related to Treg cells regulate the expression of signal transducer and activator of transcription 5 (STAT5), phospholipase D1 (PLD1), homeodomain-only protein X (HOPX), and runt-related transcription factor 3 (RUNX3) through competitive binding of miRNA or trans-regulatory mechanism, thereby regulating the differentiation and development of Treg cell.
Conclusions
The lncRNA expression profiles were changed in SLE patients, the differentially expressed lncRNAs were associated with abnormal number and function of Treg cells in SLE, and Treg-associated lncRNAs were associated with SLE-disease activity, which may affect the expression of STAT5, PLD1, HOPX, RUNX3 and regulate Treg cell function and participate in the pathogenesis and progression of SLE by competitively binding to miRNAs or trans-regulatory mechanism.
Key points
• Systemic lupus erythematosus (SLE) is an autoimmune disease involving multiple organs and systems. lncRNAs may affect Treg cells function by regulating genes expression, which may be an important pathogenesis of SLE.
• This study, taking SLE as an example, preliminarily analyzed the correlation between lncRNA and Treg cells in SLE patients, analyzed the correlation between Treg-related lncRNA and the clinical characteristics of SLE, and speculated that lncRNA could regulate the differentiation and development of Treg cells through competitive combination with miRNA or trans-regulatory mechanisms.
• It is possible to target epigenetic therapy for SLE.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>38253780</pmid><doi>10.1007/s10067-023-06844-w</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-5053-9651</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0770-3198 |
| ispartof | Clinical rheumatology, 2024-03, Vol.43 (3), p.993-1002 |
| issn | 0770-3198 1434-9949 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2917860120 |
| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Autoimmune diseases blood Cell differentiation Cell number Epigenetics Homeobox Humans Leukocytes (mononuclear) Lupus lupus erythematosus Lupus Erythematosus, Systemic Lymphocytes T Medicine Medicine & Public Health microRNA MicroRNAs MicroRNAs - genetics miRNA Non-coding RNA Original Article Pathogenesis Patients people Peripheral blood Phospholipase D1 phospholipases Protein X Rheumatology RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Runx3 protein signal transduction Stat5 protein STAT5 Transcription Factor - metabolism Systemic lupus erythematosus T-Lymphocytes, Regulatory therapeutics transactivators transcriptome Transcriptomes |
| title | Study on the expression changes of lncRNA in patients with systemic lupus erythematosus and its correlation with Treg cells |
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