lncRNAs dysregulation in monocytes from primary antiphospholipid syndrome patients: a bioinformatic and an experimental proof-of-concept approach
Background Antiphospholipid syndrome (APS) is the main cause of acquired thrombophilia where peripheral circulating cells such as monocytes have a key role. Currently, several studies have linked long non-coding RNAs (lncRNAs) in different inflammatory and autoimmune processes, including lupus. Howe...
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| Veröffentlicht in: | Molecular biology reports 2023, Vol.50 (1), p.937-941 |
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| creator | Guzmán-Martín, Carlos A. Juárez-Vicuña, Yaneli Domínguez-López, Aarón González-Ramírez, Javier Amezcua-Guerra, Luis M. Martínez-Martínez, Laura A. Sánchez-Muñoz, Fausto |
| description | Background
Antiphospholipid syndrome (APS) is the main cause of acquired thrombophilia where peripheral circulating cells such as monocytes have a key role. Currently, several studies have linked long non-coding RNAs (lncRNAs) in different inflammatory and autoimmune processes, including lupus. However, the role of lncRNAs in antiphospholipid syndrome is unknown, therefore, we aimed to select and measure expression levels of three lncRNAs based on its abundance in monocytes from APS patients.
Methods
Selection of lncRNAs candidates were carried out based on its abundance in monocytes and their relationship with Perez-Sanchez miRNA signature by using miRNet 2.0 bioinformatic tool, then lncRNAs expression levels was measured in monocytes by RT-qPCR.
Results
This is the first study to report that lncRNAs: FGD5-AS1, OIP5-AS1 and GAS5 are promising candidates for play a role on APS monocytes and they are expressed differently between patients and controls.
Conclusions
OIP5-AS1, FGD5-AS1 and GAS5 are downregulated on monocytes from APS patients. |
| doi_str_mv | 10.1007/s11033-022-08080-y |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2735868864</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2735868864</sourcerecordid><originalsourceid>FETCH-LOGICAL-c408t-4c3424b2a3376ac1a0139e75c936968ca160541b51f2bd9296eed1f82bfc00773</originalsourceid><addsrcrecordid>eNqFkc1q3TAQhUVpaG5u-wJdFEE33ajVnyU5uxDaphAaCMlayLKcKNiSa9lQP0beOJPe2xaySJBGgtE3Z9AchN4z-plRqr8UxqgQhHJOqIFF1ldowyotiKy1eY02VFBGpKnYIToq5Y5SKpmu3qBDoYTSSrENuu-Tv_x5UnC7lincLL2bY044JjzklP06h4K7KQ94nOLgphW7NMfxNheIPo6xxWVNLQABj1Aa0lyOscNNzDF1eRog56GmhcDh9xhABRjXg17OHYHtc_JhnLEbIeX87Vt00Lm-hHf7e4uuv329Oj0j5xfff5yenBMvqZmJ9EJy2XAnhFbOM0eZqIOufC1UrYx3TNFKsqZiHW_amtcqhJZ1hjedh-FpsUWfdrrQ9tcSymyHWHzoe5dCXorlRtam1qD2MqpFZZQxSgL68Ql6l5cpwUeA0lRoZuDcIr6j_JQLzL2z-_FaRu2jt3bnrQVv7R9v7QpFH_bSSzOE9l_JXzMBEDugwFO6CdP_3s_IPgAng7IK</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2770371870</pqid></control><display><type>article</type><title>lncRNAs dysregulation in monocytes from primary antiphospholipid syndrome patients: a bioinformatic and an experimental proof-of-concept approach</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Guzmán-Martín, Carlos A. ; Juárez-Vicuña, Yaneli ; Domínguez-López, Aarón ; González-Ramírez, Javier ; Amezcua-Guerra, Luis M. ; Martínez-Martínez, Laura A. ; Sánchez-Muñoz, Fausto</creator><creatorcontrib>Guzmán-Martín, Carlos A. ; Juárez-Vicuña, Yaneli ; Domínguez-López, Aarón ; González-Ramírez, Javier ; Amezcua-Guerra, Luis M. ; Martínez-Martínez, Laura A. ; Sánchez-Muñoz, Fausto</creatorcontrib><description>Background
Antiphospholipid syndrome (APS) is the main cause of acquired thrombophilia where peripheral circulating cells such as monocytes have a key role. Currently, several studies have linked long non-coding RNAs (lncRNAs) in different inflammatory and autoimmune processes, including lupus. However, the role of lncRNAs in antiphospholipid syndrome is unknown, therefore, we aimed to select and measure expression levels of three lncRNAs based on its abundance in monocytes from APS patients.
Methods
Selection of lncRNAs candidates were carried out based on its abundance in monocytes and their relationship with Perez-Sanchez miRNA signature by using miRNet 2.0 bioinformatic tool, then lncRNAs expression levels was measured in monocytes by RT-qPCR.
Results
This is the first study to report that lncRNAs: FGD5-AS1, OIP5-AS1 and GAS5 are promising candidates for play a role on APS monocytes and they are expressed differently between patients and controls.
Conclusions
OIP5-AS1, FGD5-AS1 and GAS5 are downregulated on monocytes from APS patients.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-022-08080-y</identifier><identifier>PMID: 36367661</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Animal Anatomy ; Animal Biochemistry ; Antiphospholipid syndrome ; Antiphospholipid Syndrome - genetics ; Autoimmune diseases ; Bioinformatics ; Biomedical and Life Sciences ; Computational Biology ; Histology ; Humans ; Inflammation ; Life Sciences ; Lupus ; microRNA ; MicroRNAs - genetics ; miRNA ; Molecular biology ; Monocytes ; Monocytes - metabolism ; Morphology ; Non-coding RNA ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Short Communication ; Thrombophilia ; Thrombosis</subject><ispartof>Molecular biology reports, 2023, Vol.50 (1), p.937-941</ispartof><rights>The Author(s), under exclusive licence to Springer Nature B.V. 2022</rights><rights>2022. The Author(s), under exclusive licence to Springer Nature B.V.</rights><rights>The Author(s), under exclusive licence to Springer Nature B.V. 2022.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c408t-4c3424b2a3376ac1a0139e75c936968ca160541b51f2bd9296eed1f82bfc00773</citedby><cites>FETCH-LOGICAL-c408t-4c3424b2a3376ac1a0139e75c936968ca160541b51f2bd9296eed1f82bfc00773</cites><orcidid>0000-0001-7365-9023 ; 0000-0003-4763-6578 ; 0000-0001-6556-1632 ; 0000-0001-7439-2615 ; 0000-0002-7541-8773 ; 0000-0002-6258-5732 ; 0000-0002-6467-6638</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/s11033-022-08080-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11033-022-08080-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36367661$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guzmán-Martín, Carlos A.</creatorcontrib><creatorcontrib>Juárez-Vicuña, Yaneli</creatorcontrib><creatorcontrib>Domínguez-López, Aarón</creatorcontrib><creatorcontrib>González-Ramírez, Javier</creatorcontrib><creatorcontrib>Amezcua-Guerra, Luis M.</creatorcontrib><creatorcontrib>Martínez-Martínez, Laura A.</creatorcontrib><creatorcontrib>Sánchez-Muñoz, Fausto</creatorcontrib><title>lncRNAs dysregulation in monocytes from primary antiphospholipid syndrome patients: a bioinformatic and an experimental proof-of-concept approach</title><title>Molecular biology reports</title><addtitle>Mol Biol Rep</addtitle><addtitle>Mol Biol Rep</addtitle><description>Background
Antiphospholipid syndrome (APS) is the main cause of acquired thrombophilia where peripheral circulating cells such as monocytes have a key role. Currently, several studies have linked long non-coding RNAs (lncRNAs) in different inflammatory and autoimmune processes, including lupus. However, the role of lncRNAs in antiphospholipid syndrome is unknown, therefore, we aimed to select and measure expression levels of three lncRNAs based on its abundance in monocytes from APS patients.
Methods
Selection of lncRNAs candidates were carried out based on its abundance in monocytes and their relationship with Perez-Sanchez miRNA signature by using miRNet 2.0 bioinformatic tool, then lncRNAs expression levels was measured in monocytes by RT-qPCR.
Results
This is the first study to report that lncRNAs: FGD5-AS1, OIP5-AS1 and GAS5 are promising candidates for play a role on APS monocytes and they are expressed differently between patients and controls.
Conclusions
OIP5-AS1, FGD5-AS1 and GAS5 are downregulated on monocytes from APS patients.</description><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Antiphospholipid syndrome</subject><subject>Antiphospholipid Syndrome - genetics</subject><subject>Autoimmune diseases</subject><subject>Bioinformatics</subject><subject>Biomedical and Life Sciences</subject><subject>Computational Biology</subject><subject>Histology</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Life Sciences</subject><subject>Lupus</subject><subject>microRNA</subject><subject>MicroRNAs - genetics</subject><subject>miRNA</subject><subject>Molecular biology</subject><subject>Monocytes</subject><subject>Monocytes - metabolism</subject><subject>Morphology</subject><subject>Non-coding RNA</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Short Communication</subject><subject>Thrombophilia</subject><subject>Thrombosis</subject><issn>0301-4851</issn><issn>1573-4978</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkc1q3TAQhUVpaG5u-wJdFEE33ajVnyU5uxDaphAaCMlayLKcKNiSa9lQP0beOJPe2xaySJBGgtE3Z9AchN4z-plRqr8UxqgQhHJOqIFF1ldowyotiKy1eY02VFBGpKnYIToq5Y5SKpmu3qBDoYTSSrENuu-Tv_x5UnC7lincLL2bY044JjzklP06h4K7KQ94nOLgphW7NMfxNheIPo6xxWVNLQABj1Aa0lyOscNNzDF1eRog56GmhcDh9xhABRjXg17OHYHtc_JhnLEbIeX87Vt00Lm-hHf7e4uuv329Oj0j5xfff5yenBMvqZmJ9EJy2XAnhFbOM0eZqIOufC1UrYx3TNFKsqZiHW_amtcqhJZ1hjedh-FpsUWfdrrQ9tcSymyHWHzoe5dCXorlRtam1qD2MqpFZZQxSgL68Ql6l5cpwUeA0lRoZuDcIr6j_JQLzL2z-_FaRu2jt3bnrQVv7R9v7QpFH_bSSzOE9l_JXzMBEDugwFO6CdP_3s_IPgAng7IK</recordid><startdate>2023</startdate><enddate>2023</enddate><creator>Guzmán-Martín, Carlos A.</creator><creator>Juárez-Vicuña, Yaneli</creator><creator>Domínguez-López, Aarón</creator><creator>González-Ramírez, Javier</creator><creator>Amezcua-Guerra, Luis M.</creator><creator>Martínez-Martínez, Laura A.</creator><creator>Sánchez-Muñoz, Fausto</creator><general>Springer Netherlands</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>3V.</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>7S9</scope><scope>L.6</scope><orcidid>https://orcid.org/0000-0001-7365-9023</orcidid><orcidid>https://orcid.org/0000-0003-4763-6578</orcidid><orcidid>https://orcid.org/0000-0001-6556-1632</orcidid><orcidid>https://orcid.org/0000-0001-7439-2615</orcidid><orcidid>https://orcid.org/0000-0002-7541-8773</orcidid><orcidid>https://orcid.org/0000-0002-6258-5732</orcidid><orcidid>https://orcid.org/0000-0002-6467-6638</orcidid></search><sort><creationdate>2023</creationdate><title>lncRNAs dysregulation in monocytes from primary antiphospholipid syndrome patients: a bioinformatic and an experimental proof-of-concept approach</title><author>Guzmán-Martín, Carlos A. ; Juárez-Vicuña, Yaneli ; Domínguez-López, Aarón ; González-Ramírez, Javier ; Amezcua-Guerra, Luis M. ; Martínez-Martínez, Laura A. ; Sánchez-Muñoz, Fausto</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c408t-4c3424b2a3376ac1a0139e75c936968ca160541b51f2bd9296eed1f82bfc00773</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Antiphospholipid syndrome</topic><topic>Antiphospholipid Syndrome - genetics</topic><topic>Autoimmune diseases</topic><topic>Bioinformatics</topic><topic>Biomedical and Life Sciences</topic><topic>Computational Biology</topic><topic>Histology</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Life Sciences</topic><topic>Lupus</topic><topic>microRNA</topic><topic>MicroRNAs - genetics</topic><topic>miRNA</topic><topic>Molecular biology</topic><topic>Monocytes</topic><topic>Monocytes - metabolism</topic><topic>Morphology</topic><topic>Non-coding RNA</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Short Communication</topic><topic>Thrombophilia</topic><topic>Thrombosis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guzmán-Martín, Carlos A.</creatorcontrib><creatorcontrib>Juárez-Vicuña, Yaneli</creatorcontrib><creatorcontrib>Domínguez-López, Aarón</creatorcontrib><creatorcontrib>González-Ramírez, Javier</creatorcontrib><creatorcontrib>Amezcua-Guerra, Luis M.</creatorcontrib><creatorcontrib>Martínez-Martínez, Laura A.</creatorcontrib><creatorcontrib>Sánchez-Muñoz, Fausto</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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 Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>Molecular biology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guzmán-Martín, Carlos A.</au><au>Juárez-Vicuña, Yaneli</au><au>Domínguez-López, Aarón</au><au>González-Ramírez, Javier</au><au>Amezcua-Guerra, Luis M.</au><au>Martínez-Martínez, Laura A.</au><au>Sánchez-Muñoz, Fausto</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>lncRNAs dysregulation in monocytes from primary antiphospholipid syndrome patients: a bioinformatic and an experimental proof-of-concept approach</atitle><jtitle>Molecular biology reports</jtitle><stitle>Mol Biol Rep</stitle><addtitle>Mol Biol Rep</addtitle><date>2023</date><risdate>2023</risdate><volume>50</volume><issue>1</issue><spage>937</spage><epage>941</epage><pages>937-941</pages><issn>0301-4851</issn><eissn>1573-4978</eissn><abstract>Background
Antiphospholipid syndrome (APS) is the main cause of acquired thrombophilia where peripheral circulating cells such as monocytes have a key role. Currently, several studies have linked long non-coding RNAs (lncRNAs) in different inflammatory and autoimmune processes, including lupus. However, the role of lncRNAs in antiphospholipid syndrome is unknown, therefore, we aimed to select and measure expression levels of three lncRNAs based on its abundance in monocytes from APS patients.
Methods
Selection of lncRNAs candidates were carried out based on its abundance in monocytes and their relationship with Perez-Sanchez miRNA signature by using miRNet 2.0 bioinformatic tool, then lncRNAs expression levels was measured in monocytes by RT-qPCR.
Results
This is the first study to report that lncRNAs: FGD5-AS1, OIP5-AS1 and GAS5 are promising candidates for play a role on APS monocytes and they are expressed differently between patients and controls.
Conclusions
OIP5-AS1, FGD5-AS1 and GAS5 are downregulated on monocytes from APS patients.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>36367661</pmid><doi>10.1007/s11033-022-08080-y</doi><tpages>5</tpages><orcidid>https://orcid.org/0000-0001-7365-9023</orcidid><orcidid>https://orcid.org/0000-0003-4763-6578</orcidid><orcidid>https://orcid.org/0000-0001-6556-1632</orcidid><orcidid>https://orcid.org/0000-0001-7439-2615</orcidid><orcidid>https://orcid.org/0000-0002-7541-8773</orcidid><orcidid>https://orcid.org/0000-0002-6258-5732</orcidid><orcidid>https://orcid.org/0000-0002-6467-6638</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0301-4851 |
| ispartof | Molecular biology reports, 2023, Vol.50 (1), p.937-941 |
| issn | 0301-4851 1573-4978 |
| language | eng |
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| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Animal Anatomy Animal Biochemistry Antiphospholipid syndrome Antiphospholipid Syndrome - genetics Autoimmune diseases Bioinformatics Biomedical and Life Sciences Computational Biology Histology Humans Inflammation Life Sciences Lupus microRNA MicroRNAs - genetics miRNA Molecular biology Monocytes Monocytes - metabolism Morphology Non-coding RNA RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Short Communication Thrombophilia Thrombosis |
| title | lncRNAs dysregulation in monocytes from primary antiphospholipid syndrome patients: a bioinformatic and an experimental proof-of-concept approach |
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