Lipocalin (LCN) 2 Mediates Pro-Atherosclerotic Processes and Is Elevated in Patients with Coronary Artery Disease
Lipocalin (LCN) 2 is associated with multiple acute and chronic inflammatory diseases but the underlying molecular and cellular mechanisms remain unclear. Here, we investigated whether LCN2 is released from macrophages and contributes to pro-atherosclerotic processes and whether LCN2 plasma levels a...
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| Veröffentlicht in: | PloS one 2015-09, Vol.10 (9), p.e0137924-e0137924 |
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| creator | Oberoi, Raghav Bogalle, Eskindir P Matthes, Lukas A Schuett, Harald Koch, Ann-Kathrin Grote, Karsten Schieffer, Bernhard Schuett, Jutta Luchtefeld, Maren |
| description | Lipocalin (LCN) 2 is associated with multiple acute and chronic inflammatory diseases but the underlying molecular and cellular mechanisms remain unclear. Here, we investigated whether LCN2 is released from macrophages and contributes to pro-atherosclerotic processes and whether LCN2 plasma levels are associated with the severity of coronary artery disease progression in humans.
In an autocrine-paracrine loop, tumor necrosis factor (TNF)-α promoted the release of LCN2 from murine bone-marrow derived macrophages (BMDM) and vice versa. Moreover, LCN2 stimulation of BMDM led to up-regulation of M1 macrophage markers. In addition, enhanced migration of monocytic J774A.1 cells towards LCN2 was observed. Furthermore, LCN2 increased the expression of the scavenger receptors Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) as well as scavenger receptor class A-1 (SRA-1) and induced the conversion of macrophages to foam cells. In atherosclerotic lesions of low density lipoprotein receptor-deficient (ldlr-/-) mice fed a high fat, high cholesterol diet, LCN2 was found to be co-localized with macrophages in the shoulder region of the atherosclerotic plaque. In addition, LCN2 plasma levels were significantly increased in plasma samples of these mice. Finally, LCN2 plasma levels correlated with the severity of coronary artery disease (CAD) in patients as determined by coronary angiography.
Here we demonstrated that LCN2 plays a pivotal role in processes involved in atherogenesis by promoting polarization and migration of monocytic cells and development of macrophages towards foam cells. Moreover, LCN2 may be used as a prognostic marker to determine the status of CAD progression. |
| doi_str_mv | 10.1371/journal.pone.0137924 |
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In an autocrine-paracrine loop, tumor necrosis factor (TNF)-α promoted the release of LCN2 from murine bone-marrow derived macrophages (BMDM) and vice versa. Moreover, LCN2 stimulation of BMDM led to up-regulation of M1 macrophage markers. In addition, enhanced migration of monocytic J774A.1 cells towards LCN2 was observed. Furthermore, LCN2 increased the expression of the scavenger receptors Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) as well as scavenger receptor class A-1 (SRA-1) and induced the conversion of macrophages to foam cells. In atherosclerotic lesions of low density lipoprotein receptor-deficient (ldlr-/-) mice fed a high fat, high cholesterol diet, LCN2 was found to be co-localized with macrophages in the shoulder region of the atherosclerotic plaque. In addition, LCN2 plasma levels were significantly increased in plasma samples of these mice. Finally, LCN2 plasma levels correlated with the severity of coronary artery disease (CAD) in patients as determined by coronary angiography.
Here we demonstrated that LCN2 plays a pivotal role in processes involved in atherogenesis by promoting polarization and migration of monocytic cells and development of macrophages towards foam cells. Moreover, LCN2 may be used as a prognostic marker to determine the status of CAD progression.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0137924</identifier><identifier>PMID: 26367277</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Acute-Phase Proteins - genetics ; Airway systems ; Angiography ; Animal sciences ; Animals ; Arteriosclerosis ; Atherogenesis ; Atherosclerosis ; Autocrine signalling ; Bone marrow ; Bone Marrow Cells - metabolism ; Bone Marrow Cells - pathology ; Cardiac patients ; Cardiology ; Cardiovascular disease ; Cell Line ; Cell migration ; Cholesterol ; Coronary Angiography ; Coronary artery ; Coronary artery disease ; Coronary Artery Disease - blood ; Coronary Artery Disease - diagnostic imaging ; Coronary Artery Disease - genetics ; Coronary heart disease ; Coronary vessels ; Cytokines ; Female ; Foam ; Foam Cells - metabolism ; Foam Cells - pathology ; Foams ; Heart attacks ; Heart diseases ; High cholesterol diet ; High fat diet ; Hostages ; Humans ; Inflammation ; Inflammatory diseases ; Laboratory animals ; Lectins ; Lesions ; Lipocalin ; Lipocalin-2 ; Lipocalins - blood ; Lipocalins - genetics ; Lipoprotein (low density) receptors ; Lipoproteins ; Lipoproteins (low density) ; Liquid oxygen ; Low density lipoprotein ; Low density lipoprotein receptors ; Low density lipoproteins ; LOX-1 protein ; Macrophages ; Male ; Medical schools ; Mice ; Mice, Knockout ; Monocytes ; Neutrophils ; Oncogene Proteins - blood ; Oncogene Proteins - genetics ; Paracrine signalling ; Patients ; Plasma levels ; Proto-Oncogene Proteins - blood ; Proto-Oncogene Proteins - genetics ; Receptor density ; Receptors ; Receptors, LDL - genetics ; Receptors, LDL - metabolism ; Rodents ; Scavenger receptors ; Scavenger Receptors, Class A - genetics ; Scavenger Receptors, Class A - metabolism ; Scavenger Receptors, Class E - genetics ; Scavenger Receptors, Class E - metabolism ; Smooth muscle ; TNF inhibitors ; Tumor necrosis factor ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Zoology</subject><ispartof>PloS one, 2015-09, Vol.10 (9), p.e0137924-e0137924</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Oberoi et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Oberoi et al 2015 Oberoi et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c593t-5f60856a09604185bdbc0965c944375197e498bdc9f6314e1c77784ba7906f773</citedby><cites>FETCH-LOGICAL-c593t-5f60856a09604185bdbc0965c944375197e498bdc9f6314e1c77784ba7906f773</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4569430/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4569430/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26367277$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Hsieh, Yi-Hsien</contributor><creatorcontrib>Oberoi, Raghav</creatorcontrib><creatorcontrib>Bogalle, Eskindir P</creatorcontrib><creatorcontrib>Matthes, Lukas A</creatorcontrib><creatorcontrib>Schuett, Harald</creatorcontrib><creatorcontrib>Koch, Ann-Kathrin</creatorcontrib><creatorcontrib>Grote, Karsten</creatorcontrib><creatorcontrib>Schieffer, Bernhard</creatorcontrib><creatorcontrib>Schuett, Jutta</creatorcontrib><creatorcontrib>Luchtefeld, Maren</creatorcontrib><title>Lipocalin (LCN) 2 Mediates Pro-Atherosclerotic Processes and Is Elevated in Patients with Coronary Artery Disease</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Lipocalin (LCN) 2 is associated with multiple acute and chronic inflammatory diseases but the underlying molecular and cellular mechanisms remain unclear. Here, we investigated whether LCN2 is released from macrophages and contributes to pro-atherosclerotic processes and whether LCN2 plasma levels are associated with the severity of coronary artery disease progression in humans.
In an autocrine-paracrine loop, tumor necrosis factor (TNF)-α promoted the release of LCN2 from murine bone-marrow derived macrophages (BMDM) and vice versa. Moreover, LCN2 stimulation of BMDM led to up-regulation of M1 macrophage markers. In addition, enhanced migration of monocytic J774A.1 cells towards LCN2 was observed. Furthermore, LCN2 increased the expression of the scavenger receptors Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) as well as scavenger receptor class A-1 (SRA-1) and induced the conversion of macrophages to foam cells. In atherosclerotic lesions of low density lipoprotein receptor-deficient (ldlr-/-) mice fed a high fat, high cholesterol diet, LCN2 was found to be co-localized with macrophages in the shoulder region of the atherosclerotic plaque. In addition, LCN2 plasma levels were significantly increased in plasma samples of these mice. Finally, LCN2 plasma levels correlated with the severity of coronary artery disease (CAD) in patients as determined by coronary angiography.
Here we demonstrated that LCN2 plays a pivotal role in processes involved in atherogenesis by promoting polarization and migration of monocytic cells and development of macrophages towards foam cells. Moreover, LCN2 may be used as a prognostic marker to determine the status of CAD progression.</description><subject>Acute-Phase Proteins - genetics</subject><subject>Airway systems</subject><subject>Angiography</subject><subject>Animal sciences</subject><subject>Animals</subject><subject>Arteriosclerosis</subject><subject>Atherogenesis</subject><subject>Atherosclerosis</subject><subject>Autocrine signalling</subject><subject>Bone marrow</subject><subject>Bone Marrow Cells - metabolism</subject><subject>Bone Marrow Cells - pathology</subject><subject>Cardiac patients</subject><subject>Cardiology</subject><subject>Cardiovascular disease</subject><subject>Cell Line</subject><subject>Cell migration</subject><subject>Cholesterol</subject><subject>Coronary Angiography</subject><subject>Coronary artery</subject><subject>Coronary artery disease</subject><subject>Coronary Artery Disease - blood</subject><subject>Coronary Artery Disease - diagnostic imaging</subject><subject>Coronary Artery Disease - genetics</subject><subject>Coronary heart disease</subject><subject>Coronary vessels</subject><subject>Cytokines</subject><subject>Female</subject><subject>Foam</subject><subject>Foam Cells - metabolism</subject><subject>Foam Cells - pathology</subject><subject>Foams</subject><subject>Heart attacks</subject><subject>Heart diseases</subject><subject>High cholesterol diet</subject><subject>High fat diet</subject><subject>Hostages</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammatory diseases</subject><subject>Laboratory animals</subject><subject>Lectins</subject><subject>Lesions</subject><subject>Lipocalin</subject><subject>Lipocalin-2</subject><subject>Lipocalins - blood</subject><subject>Lipocalins - genetics</subject><subject>Lipoprotein (low density) receptors</subject><subject>Lipoproteins</subject><subject>Lipoproteins (low density)</subject><subject>Liquid oxygen</subject><subject>Low density lipoprotein</subject><subject>Low density lipoprotein receptors</subject><subject>Low density lipoproteins</subject><subject>LOX-1 protein</subject><subject>Macrophages</subject><subject>Male</subject><subject>Medical schools</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Monocytes</subject><subject>Neutrophils</subject><subject>Oncogene Proteins - 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genetics</topic><topic>Scavenger Receptors, Class A - metabolism</topic><topic>Scavenger Receptors, Class E - genetics</topic><topic>Scavenger Receptors, Class E - metabolism</topic><topic>Smooth muscle</topic><topic>TNF inhibitors</topic><topic>Tumor necrosis factor</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><topic>Zoology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Oberoi, Raghav</creatorcontrib><creatorcontrib>Bogalle, Eskindir P</creatorcontrib><creatorcontrib>Matthes, Lukas A</creatorcontrib><creatorcontrib>Schuett, Harald</creatorcontrib><creatorcontrib>Koch, Ann-Kathrin</creatorcontrib><creatorcontrib>Grote, Karsten</creatorcontrib><creatorcontrib>Schieffer, Bernhard</creatorcontrib><creatorcontrib>Schuett, Jutta</creatorcontrib><creatorcontrib>Luchtefeld, Maren</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>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</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>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Oberoi, Raghav</au><au>Bogalle, Eskindir P</au><au>Matthes, Lukas A</au><au>Schuett, Harald</au><au>Koch, Ann-Kathrin</au><au>Grote, Karsten</au><au>Schieffer, Bernhard</au><au>Schuett, Jutta</au><au>Luchtefeld, Maren</au><au>Hsieh, Yi-Hsien</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lipocalin (LCN) 2 Mediates Pro-Atherosclerotic Processes and Is Elevated in Patients with Coronary Artery Disease</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-09-14</date><risdate>2015</risdate><volume>10</volume><issue>9</issue><spage>e0137924</spage><epage>e0137924</epage><pages>e0137924-e0137924</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Lipocalin (LCN) 2 is associated with multiple acute and chronic inflammatory diseases but the underlying molecular and cellular mechanisms remain unclear. Here, we investigated whether LCN2 is released from macrophages and contributes to pro-atherosclerotic processes and whether LCN2 plasma levels are associated with the severity of coronary artery disease progression in humans.
In an autocrine-paracrine loop, tumor necrosis factor (TNF)-α promoted the release of LCN2 from murine bone-marrow derived macrophages (BMDM) and vice versa. Moreover, LCN2 stimulation of BMDM led to up-regulation of M1 macrophage markers. In addition, enhanced migration of monocytic J774A.1 cells towards LCN2 was observed. Furthermore, LCN2 increased the expression of the scavenger receptors Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) as well as scavenger receptor class A-1 (SRA-1) and induced the conversion of macrophages to foam cells. In atherosclerotic lesions of low density lipoprotein receptor-deficient (ldlr-/-) mice fed a high fat, high cholesterol diet, LCN2 was found to be co-localized with macrophages in the shoulder region of the atherosclerotic plaque. In addition, LCN2 plasma levels were significantly increased in plasma samples of these mice. Finally, LCN2 plasma levels correlated with the severity of coronary artery disease (CAD) in patients as determined by coronary angiography.
Here we demonstrated that LCN2 plays a pivotal role in processes involved in atherogenesis by promoting polarization and migration of monocytic cells and development of macrophages towards foam cells. Moreover, LCN2 may be used as a prognostic marker to determine the status of CAD progression.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26367277</pmid><doi>10.1371/journal.pone.0137924</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2015-09, Vol.10 (9), p.e0137924-e0137924 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1719284261 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Acute-Phase Proteins - genetics Airway systems Angiography Animal sciences Animals Arteriosclerosis Atherogenesis Atherosclerosis Autocrine signalling Bone marrow Bone Marrow Cells - metabolism Bone Marrow Cells - pathology Cardiac patients Cardiology Cardiovascular disease Cell Line Cell migration Cholesterol Coronary Angiography Coronary artery Coronary artery disease Coronary Artery Disease - blood Coronary Artery Disease - diagnostic imaging Coronary Artery Disease - genetics Coronary heart disease Coronary vessels Cytokines Female Foam Foam Cells - metabolism Foam Cells - pathology Foams Heart attacks Heart diseases High cholesterol diet High fat diet Hostages Humans Inflammation Inflammatory diseases Laboratory animals Lectins Lesions Lipocalin Lipocalin-2 Lipocalins - blood Lipocalins - genetics Lipoprotein (low density) receptors Lipoproteins Lipoproteins (low density) Liquid oxygen Low density lipoprotein Low density lipoprotein receptors Low density lipoproteins LOX-1 protein Macrophages Male Medical schools Mice Mice, Knockout Monocytes Neutrophils Oncogene Proteins - blood Oncogene Proteins - genetics Paracrine signalling Patients Plasma levels Proto-Oncogene Proteins - blood Proto-Oncogene Proteins - genetics Receptor density Receptors Receptors, LDL - genetics Receptors, LDL - metabolism Rodents Scavenger receptors Scavenger Receptors, Class A - genetics Scavenger Receptors, Class A - metabolism Scavenger Receptors, Class E - genetics Scavenger Receptors, Class E - metabolism Smooth muscle TNF inhibitors Tumor necrosis factor Tumor necrosis factor-TNF Tumor necrosis factor-α Zoology |
| title | Lipocalin (LCN) 2 Mediates Pro-Atherosclerotic Processes and Is Elevated in Patients with Coronary Artery Disease |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-26T14%3A37%3A25IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Lipocalin%20(LCN)%202%20Mediates%20Pro-Atherosclerotic%20Processes%20and%20Is%20Elevated%20in%20Patients%20with%20Coronary%20Artery%20Disease&rft.jtitle=PloS%20one&rft.au=Oberoi,%20Raghav&rft.date=2015-09-14&rft.volume=10&rft.issue=9&rft.spage=e0137924&rft.epage=e0137924&rft.pages=e0137924-e0137924&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0137924&rft_dat=%3Cgale_plos_%3EA428587034%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1719284261&rft_id=info:pmid/26367277&rft_galeid=A428587034&rft_doaj_id=oai_doaj_org_article_0cc520b1b5bc4b989d6a250e373d1c47&rfr_iscdi=true |