Role of Low‐Density Lipoprotein in Early Vascular Aging Associated With Systemic Lupus Erythematosus
Objective Patients with systemic lupus erythematosus (SLE) often have atherosclerotic complications at a young age but normal low‐density lipoprotein (LDL) levels. This study was undertaken to investigate the role of LDL composition in promoting early vascular aging in SLE patients. Methods Plasma L...
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| Veröffentlicht in: | Arthritis & rheumatology (Hoboken, N.J.) N.J.), 2020-06, Vol.72 (6), p.972-984 |
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| creator | Chan, Hua‐Chen Chan, Hsiu‐Chuan Liang, Chan‐Jung Lee, Hsiang‐Chun Su, Hung Lee, An‐Sheng Shiea, Jentaie Tsai, Wen‐Chan Ou, Tsan‐Teng Wu, Cheng‐Chin Chu, Chih‐Sheng Dixon, Richard A. Ke, Liang‐Yin Yen, Jeng‐Hsien Chen, Chu‐Huang |
| description | Objective
Patients with systemic lupus erythematosus (SLE) often have atherosclerotic complications at a young age but normal low‐density lipoprotein (LDL) levels. This study was undertaken to investigate the role of LDL composition in promoting early vascular aging in SLE patients.
Methods
Plasma LDL from 45 SLE patients (SLE‐LDL) and from 37 normal healthy controls (N‐LDL) was chromatographically divided into 5 subfractions (L1–L5), and the subfraction composition was analyzed. Correlations between subfraction levels and signs of early vascular aging were assessed. Mechanisms of lipid‐mediated endothelial dysfunction were explored using in vitro assays and experiments in apoE−/− mice.
Results
The L5 percentage was increased 3.4 times in the plasma of SLE patients compared with normal controls. This increased percentage of SLE‐L5 was positively correlated with the mean blood pressure (r = 0.27, P = 0.04), carotid intima‐media thickness (IMT) (right carotid IMT, r = 0.4, P = 0.004; left carotid IMT, r = 0.36, P = 0.01), pulse wave velocity (r = 0.29, P = 0.04), and blood levels of CD16+ monocytes (r = 0.35, P = 0.004) and CX3CL1 cytokines (r = 0.43, P < 0.001) in SLE patients. Matrix‐assisted laser desorption ionization–time‐of‐flight mass spectrometry analysis revealed that plasma levels of lysophosphatidylcholine (LPC) and platelet‐activating factor (PAF) were increased in SLE‐LDL and in the SLE‐L5 plasma subfraction. Injecting SLE‐LDL, SLE‐L5, or LPC into young, male apoE−/− mice caused increases in plasma CX3CL1 levels, aortic fatty‐streak areas, aortic vascular aging, and macrophage infiltration into the aortic wall, whereas injection of N‐LDL or SLE‐L1 had negligible effects (n = 3–8 mice per group). In vitro, SLE‐L5 lipid extracts induced increases in CX3CR1 and CD16 expression in human monocytes; synthetic PAF and LPC had similar effects. Furthermore, lipid extracts of SLE‐LDL and SLE‐L5 induced the expression of CX3CL1 and enhanced monocyte–endothelial cell adhesion in assays with bovine aortic endothelial cells.
Conclusion
An increase in plasma L5 levels, not total LDL concentration, may promote early vascular aging in SLE patients, leading to premature atherosclerosis. |
| doi_str_mv | 10.1002/art.41213 |
| format | Article |
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Patients with systemic lupus erythematosus (SLE) often have atherosclerotic complications at a young age but normal low‐density lipoprotein (LDL) levels. This study was undertaken to investigate the role of LDL composition in promoting early vascular aging in SLE patients.
Methods
Plasma LDL from 45 SLE patients (SLE‐LDL) and from 37 normal healthy controls (N‐LDL) was chromatographically divided into 5 subfractions (L1–L5), and the subfraction composition was analyzed. Correlations between subfraction levels and signs of early vascular aging were assessed. Mechanisms of lipid‐mediated endothelial dysfunction were explored using in vitro assays and experiments in apoE−/− mice.
Results
The L5 percentage was increased 3.4 times in the plasma of SLE patients compared with normal controls. This increased percentage of SLE‐L5 was positively correlated with the mean blood pressure (r = 0.27, P = 0.04), carotid intima‐media thickness (IMT) (right carotid IMT, r = 0.4, P = 0.004; left carotid IMT, r = 0.36, P = 0.01), pulse wave velocity (r = 0.29, P = 0.04), and blood levels of CD16+ monocytes (r = 0.35, P = 0.004) and CX3CL1 cytokines (r = 0.43, P < 0.001) in SLE patients. Matrix‐assisted laser desorption ionization–time‐of‐flight mass spectrometry analysis revealed that plasma levels of lysophosphatidylcholine (LPC) and platelet‐activating factor (PAF) were increased in SLE‐LDL and in the SLE‐L5 plasma subfraction. Injecting SLE‐LDL, SLE‐L5, or LPC into young, male apoE−/− mice caused increases in plasma CX3CL1 levels, aortic fatty‐streak areas, aortic vascular aging, and macrophage infiltration into the aortic wall, whereas injection of N‐LDL or SLE‐L1 had negligible effects (n = 3–8 mice per group). In vitro, SLE‐L5 lipid extracts induced increases in CX3CR1 and CD16 expression in human monocytes; synthetic PAF and LPC had similar effects. Furthermore, lipid extracts of SLE‐LDL and SLE‐L5 induced the expression of CX3CL1 and enhanced monocyte–endothelial cell adhesion in assays with bovine aortic endothelial cells.
Conclusion
An increase in plasma L5 levels, not total LDL concentration, may promote early vascular aging in SLE patients, leading to premature atherosclerosis.</description><identifier>ISSN: 2326-5191</identifier><identifier>EISSN: 2326-5205</identifier><identifier>DOI: 10.1002/art.41213</identifier><identifier>PMID: 31994323</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Aging ; Aorta ; Apolipoprotein E ; Arteriosclerosis ; Atherosclerosis ; Blood levels ; Blood pressure ; CD16 antigen ; Cell adhesion ; Cell adhesion & migration ; Chronic conditions ; Complications ; Composition ; Correlation analysis ; CX3CR1 protein ; Cytokines ; Density ; Endothelial cells ; Ionization ; Lipids ; Low density lipoprotein ; Lupus ; Lysophosphatidylcholine ; Macrophages ; Mass spectrometry ; Mass spectroscopy ; Monocytes ; Plasma ; Plasma levels ; Platelet-activating factor ; Systemic lupus erythematosus ; Wave velocity</subject><ispartof>Arthritis & rheumatology (Hoboken, N.J.), 2020-06, Vol.72 (6), p.972-984</ispartof><rights>2020, American College of Rheumatology</rights><rights>2020, American College of Rheumatology.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3533-18d6a89b989da776dd4ace346b212c66cf180d33c08bfd89cd26d7bb0fd3d0d13</citedby><cites>FETCH-LOGICAL-c3533-18d6a89b989da776dd4ace346b212c66cf180d33c08bfd89cd26d7bb0fd3d0d13</cites><orcidid>0000-0002-1509-7883 ; 0000-0001-8176-3269 ; 0000-0002-2547-0987 ; 0000-0001-7016-8392</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%2Fart.41213$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fart.41213$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31994323$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chan, Hua‐Chen</creatorcontrib><creatorcontrib>Chan, Hsiu‐Chuan</creatorcontrib><creatorcontrib>Liang, Chan‐Jung</creatorcontrib><creatorcontrib>Lee, Hsiang‐Chun</creatorcontrib><creatorcontrib>Su, Hung</creatorcontrib><creatorcontrib>Lee, An‐Sheng</creatorcontrib><creatorcontrib>Shiea, Jentaie</creatorcontrib><creatorcontrib>Tsai, Wen‐Chan</creatorcontrib><creatorcontrib>Ou, Tsan‐Teng</creatorcontrib><creatorcontrib>Wu, Cheng‐Chin</creatorcontrib><creatorcontrib>Chu, Chih‐Sheng</creatorcontrib><creatorcontrib>Dixon, Richard A.</creatorcontrib><creatorcontrib>Ke, Liang‐Yin</creatorcontrib><creatorcontrib>Yen, Jeng‐Hsien</creatorcontrib><creatorcontrib>Chen, Chu‐Huang</creatorcontrib><title>Role of Low‐Density Lipoprotein in Early Vascular Aging Associated With Systemic Lupus Erythematosus</title><title>Arthritis & rheumatology (Hoboken, N.J.)</title><addtitle>Arthritis Rheumatol</addtitle><description>Objective
Patients with systemic lupus erythematosus (SLE) often have atherosclerotic complications at a young age but normal low‐density lipoprotein (LDL) levels. This study was undertaken to investigate the role of LDL composition in promoting early vascular aging in SLE patients.
Methods
Plasma LDL from 45 SLE patients (SLE‐LDL) and from 37 normal healthy controls (N‐LDL) was chromatographically divided into 5 subfractions (L1–L5), and the subfraction composition was analyzed. Correlations between subfraction levels and signs of early vascular aging were assessed. Mechanisms of lipid‐mediated endothelial dysfunction were explored using in vitro assays and experiments in apoE−/− mice.
Results
The L5 percentage was increased 3.4 times in the plasma of SLE patients compared with normal controls. This increased percentage of SLE‐L5 was positively correlated with the mean blood pressure (r = 0.27, P = 0.04), carotid intima‐media thickness (IMT) (right carotid IMT, r = 0.4, P = 0.004; left carotid IMT, r = 0.36, P = 0.01), pulse wave velocity (r = 0.29, P = 0.04), and blood levels of CD16+ monocytes (r = 0.35, P = 0.004) and CX3CL1 cytokines (r = 0.43, P < 0.001) in SLE patients. Matrix‐assisted laser desorption ionization–time‐of‐flight mass spectrometry analysis revealed that plasma levels of lysophosphatidylcholine (LPC) and platelet‐activating factor (PAF) were increased in SLE‐LDL and in the SLE‐L5 plasma subfraction. Injecting SLE‐LDL, SLE‐L5, or LPC into young, male apoE−/− mice caused increases in plasma CX3CL1 levels, aortic fatty‐streak areas, aortic vascular aging, and macrophage infiltration into the aortic wall, whereas injection of N‐LDL or SLE‐L1 had negligible effects (n = 3–8 mice per group). In vitro, SLE‐L5 lipid extracts induced increases in CX3CR1 and CD16 expression in human monocytes; synthetic PAF and LPC had similar effects. Furthermore, lipid extracts of SLE‐LDL and SLE‐L5 induced the expression of CX3CL1 and enhanced monocyte–endothelial cell adhesion in assays with bovine aortic endothelial cells.
Conclusion
An increase in plasma L5 levels, not total LDL concentration, may promote early vascular aging in SLE patients, leading to premature atherosclerosis.</description><subject>Aging</subject><subject>Aorta</subject><subject>Apolipoprotein E</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis</subject><subject>Blood levels</subject><subject>Blood pressure</subject><subject>CD16 antigen</subject><subject>Cell adhesion</subject><subject>Cell adhesion & migration</subject><subject>Chronic conditions</subject><subject>Complications</subject><subject>Composition</subject><subject>Correlation analysis</subject><subject>CX3CR1 protein</subject><subject>Cytokines</subject><subject>Density</subject><subject>Endothelial cells</subject><subject>Ionization</subject><subject>Lipids</subject><subject>Low density lipoprotein</subject><subject>Lupus</subject><subject>Lysophosphatidylcholine</subject><subject>Macrophages</subject><subject>Mass spectrometry</subject><subject>Mass spectroscopy</subject><subject>Monocytes</subject><subject>Plasma</subject><subject>Plasma levels</subject><subject>Platelet-activating factor</subject><subject>Systemic lupus erythematosus</subject><subject>Wave velocity</subject><issn>2326-5191</issn><issn>2326-5205</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNp1kMtKxDAUhoMojowufAEJuNHFaC69pMtBxwsUBK_LkCbpGGmbMUkZuvMRfEafxOiMLgQPB85ZfPz8fADsY3SCESKnwoWTBBNMN8AOoSSbpASlmz8_LvAI7Hn_guIUOcpQug1GFBdFQgndAfWtbTS0NSzt8uPt_Vx33oQBlmZhF84GbToYdyZcM8BH4WXfCAenc9PN4dR7K40IWsEnE57h3eCDbo2EZb_oPZy5ITzrVgTre78LtmrReL23vmPwcDG7P7ualDeX12fTciJpSukEM5UJVlQFK5TI80ypREhNk6wimMgskzVmSFEqEatqxQqpSKbyqkK1ogopTMfgaJUby7_22gfeGi9104hO295zQhMWVRGWRvTwD_pie9fFdpwkKEc4TRmK1PGKks5673TNF860wg0cI_7ln0f__Nt_ZA_WiX3VavVL_tiOwOkKWJpGD_8n8ent_SryE4Scj-0</recordid><startdate>202006</startdate><enddate>202006</enddate><creator>Chan, Hua‐Chen</creator><creator>Chan, Hsiu‐Chuan</creator><creator>Liang, Chan‐Jung</creator><creator>Lee, Hsiang‐Chun</creator><creator>Su, Hung</creator><creator>Lee, An‐Sheng</creator><creator>Shiea, Jentaie</creator><creator>Tsai, Wen‐Chan</creator><creator>Ou, Tsan‐Teng</creator><creator>Wu, Cheng‐Chin</creator><creator>Chu, Chih‐Sheng</creator><creator>Dixon, Richard A.</creator><creator>Ke, Liang‐Yin</creator><creator>Yen, Jeng‐Hsien</creator><creator>Chen, Chu‐Huang</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7TM</scope><scope>7U7</scope><scope>C1K</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-1509-7883</orcidid><orcidid>https://orcid.org/0000-0001-8176-3269</orcidid><orcidid>https://orcid.org/0000-0002-2547-0987</orcidid><orcidid>https://orcid.org/0000-0001-7016-8392</orcidid></search><sort><creationdate>202006</creationdate><title>Role of Low‐Density Lipoprotein in Early Vascular Aging Associated With Systemic Lupus Erythematosus</title><author>Chan, Hua‐Chen ; Chan, Hsiu‐Chuan ; Liang, Chan‐Jung ; Lee, Hsiang‐Chun ; Su, Hung ; Lee, An‐Sheng ; Shiea, Jentaie ; Tsai, Wen‐Chan ; Ou, Tsan‐Teng ; Wu, Cheng‐Chin ; Chu, Chih‐Sheng ; Dixon, Richard A. ; Ke, Liang‐Yin ; Yen, Jeng‐Hsien ; Chen, Chu‐Huang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3533-18d6a89b989da776dd4ace346b212c66cf180d33c08bfd89cd26d7bb0fd3d0d13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Aging</topic><topic>Aorta</topic><topic>Apolipoprotein E</topic><topic>Arteriosclerosis</topic><topic>Atherosclerosis</topic><topic>Blood levels</topic><topic>Blood pressure</topic><topic>CD16 antigen</topic><topic>Cell adhesion</topic><topic>Cell adhesion & migration</topic><topic>Chronic conditions</topic><topic>Complications</topic><topic>Composition</topic><topic>Correlation analysis</topic><topic>CX3CR1 protein</topic><topic>Cytokines</topic><topic>Density</topic><topic>Endothelial cells</topic><topic>Ionization</topic><topic>Lipids</topic><topic>Low density lipoprotein</topic><topic>Lupus</topic><topic>Lysophosphatidylcholine</topic><topic>Macrophages</topic><topic>Mass spectrometry</topic><topic>Mass spectroscopy</topic><topic>Monocytes</topic><topic>Plasma</topic><topic>Plasma levels</topic><topic>Platelet-activating factor</topic><topic>Systemic lupus erythematosus</topic><topic>Wave velocity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chan, Hua‐Chen</creatorcontrib><creatorcontrib>Chan, Hsiu‐Chuan</creatorcontrib><creatorcontrib>Liang, Chan‐Jung</creatorcontrib><creatorcontrib>Lee, Hsiang‐Chun</creatorcontrib><creatorcontrib>Su, Hung</creatorcontrib><creatorcontrib>Lee, An‐Sheng</creatorcontrib><creatorcontrib>Shiea, Jentaie</creatorcontrib><creatorcontrib>Tsai, Wen‐Chan</creatorcontrib><creatorcontrib>Ou, Tsan‐Teng</creatorcontrib><creatorcontrib>Wu, Cheng‐Chin</creatorcontrib><creatorcontrib>Chu, Chih‐Sheng</creatorcontrib><creatorcontrib>Dixon, Richard A.</creatorcontrib><creatorcontrib>Ke, Liang‐Yin</creatorcontrib><creatorcontrib>Yen, Jeng‐Hsien</creatorcontrib><creatorcontrib>Chen, Chu‐Huang</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Arthritis & rheumatology (Hoboken, N.J.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chan, Hua‐Chen</au><au>Chan, Hsiu‐Chuan</au><au>Liang, Chan‐Jung</au><au>Lee, Hsiang‐Chun</au><au>Su, Hung</au><au>Lee, An‐Sheng</au><au>Shiea, Jentaie</au><au>Tsai, Wen‐Chan</au><au>Ou, Tsan‐Teng</au><au>Wu, Cheng‐Chin</au><au>Chu, Chih‐Sheng</au><au>Dixon, Richard A.</au><au>Ke, Liang‐Yin</au><au>Yen, Jeng‐Hsien</au><au>Chen, Chu‐Huang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of Low‐Density Lipoprotein in Early Vascular Aging Associated With Systemic Lupus Erythematosus</atitle><jtitle>Arthritis & rheumatology (Hoboken, N.J.)</jtitle><addtitle>Arthritis Rheumatol</addtitle><date>2020-06</date><risdate>2020</risdate><volume>72</volume><issue>6</issue><spage>972</spage><epage>984</epage><pages>972-984</pages><issn>2326-5191</issn><eissn>2326-5205</eissn><abstract>Objective
Patients with systemic lupus erythematosus (SLE) often have atherosclerotic complications at a young age but normal low‐density lipoprotein (LDL) levels. This study was undertaken to investigate the role of LDL composition in promoting early vascular aging in SLE patients.
Methods
Plasma LDL from 45 SLE patients (SLE‐LDL) and from 37 normal healthy controls (N‐LDL) was chromatographically divided into 5 subfractions (L1–L5), and the subfraction composition was analyzed. Correlations between subfraction levels and signs of early vascular aging were assessed. Mechanisms of lipid‐mediated endothelial dysfunction were explored using in vitro assays and experiments in apoE−/− mice.
Results
The L5 percentage was increased 3.4 times in the plasma of SLE patients compared with normal controls. This increased percentage of SLE‐L5 was positively correlated with the mean blood pressure (r = 0.27, P = 0.04), carotid intima‐media thickness (IMT) (right carotid IMT, r = 0.4, P = 0.004; left carotid IMT, r = 0.36, P = 0.01), pulse wave velocity (r = 0.29, P = 0.04), and blood levels of CD16+ monocytes (r = 0.35, P = 0.004) and CX3CL1 cytokines (r = 0.43, P < 0.001) in SLE patients. Matrix‐assisted laser desorption ionization–time‐of‐flight mass spectrometry analysis revealed that plasma levels of lysophosphatidylcholine (LPC) and platelet‐activating factor (PAF) were increased in SLE‐LDL and in the SLE‐L5 plasma subfraction. Injecting SLE‐LDL, SLE‐L5, or LPC into young, male apoE−/− mice caused increases in plasma CX3CL1 levels, aortic fatty‐streak areas, aortic vascular aging, and macrophage infiltration into the aortic wall, whereas injection of N‐LDL or SLE‐L1 had negligible effects (n = 3–8 mice per group). In vitro, SLE‐L5 lipid extracts induced increases in CX3CR1 and CD16 expression in human monocytes; synthetic PAF and LPC had similar effects. Furthermore, lipid extracts of SLE‐LDL and SLE‐L5 induced the expression of CX3CL1 and enhanced monocyte–endothelial cell adhesion in assays with bovine aortic endothelial cells.
Conclusion
An increase in plasma L5 levels, not total LDL concentration, may promote early vascular aging in SLE patients, leading to premature atherosclerosis.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>31994323</pmid><doi>10.1002/art.41213</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-1509-7883</orcidid><orcidid>https://orcid.org/0000-0001-8176-3269</orcidid><orcidid>https://orcid.org/0000-0002-2547-0987</orcidid><orcidid>https://orcid.org/0000-0001-7016-8392</orcidid></addata></record> |
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| ispartof | Arthritis & rheumatology (Hoboken, N.J.), 2020-06, Vol.72 (6), p.972-984 |
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| source | Wiley Online Library Journals Frontfile Complete; Alma/SFX Local Collection |
| subjects | Aging Aorta Apolipoprotein E Arteriosclerosis Atherosclerosis Blood levels Blood pressure CD16 antigen Cell adhesion Cell adhesion & migration Chronic conditions Complications Composition Correlation analysis CX3CR1 protein Cytokines Density Endothelial cells Ionization Lipids Low density lipoprotein Lupus Lysophosphatidylcholine Macrophages Mass spectrometry Mass spectroscopy Monocytes Plasma Plasma levels Platelet-activating factor Systemic lupus erythematosus Wave velocity |
| title | Role of Low‐Density Lipoprotein in Early Vascular Aging Associated With Systemic Lupus Erythematosus |
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