Angiotensin II induces LOX-1, the human endothelial receptor for oxidized low-density lipoprotein
Oxidatively modified LDL (oxLDL) plays an important role in the development of atherosclerosis. OxLDL effects, eg, foam cell formation, are mediated in part by the classic scavenger receptor, whereas other effects may involve the recently cloned endothelial oxLDL receptor, LOX-1 (lectinlike oxLDL re...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 1999-08, Vol.100 (9), p.899-902 |
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| creator | MORAWIETZ, H RUECKSCHLOSS, U NIEMANN, B DUERRSCHMIDT, N GALLE, J HAKIM, K ZERKOWSKI, H.-R SAWAMURA, T HOLTZ, J |
| description | Oxidatively modified LDL (oxLDL) plays an important role in the development of atherosclerosis. OxLDL effects, eg, foam cell formation, are mediated in part by the classic scavenger receptor, whereas other effects may involve the recently cloned endothelial oxLDL receptor, LOX-1 (lectinlike oxLDL receptor-1), which is distinct from macrophage scavenger receptors. Because the regulation of LOX-1 must still be defined, we investigated whether LOX-1 is regulated by the potentially proatherosclerotic stimulant angiotensin II (Ang II).
Using competitive reverse transcription-polymerase chain reaction (RT-PCR), we quantified mRNA expression of LOX-1 in primary cultures of human umbilical vein endothelial cells (HUVECs). After treatment with Ang II for 3 hours (1 nmol/L to 1 micromol/L), LOX-1 mRNA was concentration-dependently induced (from 6.9+/-1.4 to 23.1+/-5.5 relative units [RU] by 1 micromol/L Ang II; P |
| doi_str_mv | 10.1161/01.cir.100.9.899 |
| format | Article |
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Using competitive reverse transcription-polymerase chain reaction (RT-PCR), we quantified mRNA expression of LOX-1 in primary cultures of human umbilical vein endothelial cells (HUVECs). After treatment with Ang II for 3 hours (1 nmol/L to 1 micromol/L), LOX-1 mRNA was concentration-dependently induced (from 6.9+/-1.4 to 23.1+/-5.5 relative units [RU] by 1 micromol/L Ang II; P<0.05). The angiotensin II type 1 (AT(1)) receptor antagonist losartan prevented this induction. Incubation of HUVECs with Ang II (100 nmol/L, 3 hours) induced LOX-1 protein expression (212+/-21% of control level; P<0. 01) and uptake of 1,1'-dioctadecyl-3,3,3', 3'-tetramethylindocarbocyanine perchlorate (DiI)-labeled oxLDL (209+/-17% of control level; P<0.05) by an AT(1)-dependent pathway, reaching its maximum after 24 hours (680+/-89%; P<0.05). In internal mammary artery biopsy samples from patients with or without ACE inhibitor treatment before coronary artery bypass surgery, LOX-1 mRNA was downregulated by ACE inhibition (6.4+/-2.0 versus 19.3+/-5. 9 RU; n=12 each; P<0.05).
We conclude that LOX-1 is regulated by Ang II in vitro and in vivo, that induction of LOX-1 is mediated by the AT(1) receptor, and that repression of LOX-1 by long-term ACE inhibitor treatment may contribute to the antiatherosclerotic potential of this therapy.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.cir.100.9.899</identifier><identifier>PMID: 10468518</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Angiotensin II - metabolism ; Angiotensin-Converting Enzyme Inhibitors - pharmacology ; Anti-Arrhythmia Agents - pharmacology ; Antihypertensive Agents - pharmacology ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Cells, Cultured ; Coronary Artery Bypass ; Coronary Artery Disease - drug therapy ; Coronary Artery Disease - metabolism ; Coronary Artery Disease - surgery ; Down-Regulation - drug effects ; Endothelium, Vascular - cytology ; Humans ; Losartan - pharmacology ; Mammary Arteries ; Medical sciences ; Receptors, LDL - genetics ; Receptors, LDL - metabolism ; Receptors, Oxidized LDL ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - analysis ; Scavenger Receptors, Class E ; Umbilical Veins</subject><ispartof>Circulation (New York, N.Y.), 1999-08, Vol.100 (9), p.899-902</ispartof><rights>1999 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Aug 31, 1999</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c547t-c289d35a77d486335e5b468c536fcce10ea4d371df0b3251e3a10a2004343af73</citedby><cites>FETCH-LOGICAL-c547t-c289d35a77d486335e5b468c536fcce10ea4d371df0b3251e3a10a2004343af73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>309,310,314,780,784,789,790,3687,23930,23931,25140,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1917662$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10468518$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>MORAWIETZ, H</creatorcontrib><creatorcontrib>RUECKSCHLOSS, U</creatorcontrib><creatorcontrib>NIEMANN, B</creatorcontrib><creatorcontrib>DUERRSCHMIDT, N</creatorcontrib><creatorcontrib>GALLE, J</creatorcontrib><creatorcontrib>HAKIM, K</creatorcontrib><creatorcontrib>ZERKOWSKI, H.-R</creatorcontrib><creatorcontrib>SAWAMURA, T</creatorcontrib><creatorcontrib>HOLTZ, J</creatorcontrib><title>Angiotensin II induces LOX-1, the human endothelial receptor for oxidized low-density lipoprotein</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Oxidatively modified LDL (oxLDL) plays an important role in the development of atherosclerosis. OxLDL effects, eg, foam cell formation, are mediated in part by the classic scavenger receptor, whereas other effects may involve the recently cloned endothelial oxLDL receptor, LOX-1 (lectinlike oxLDL receptor-1), which is distinct from macrophage scavenger receptors. Because the regulation of LOX-1 must still be defined, we investigated whether LOX-1 is regulated by the potentially proatherosclerotic stimulant angiotensin II (Ang II).
Using competitive reverse transcription-polymerase chain reaction (RT-PCR), we quantified mRNA expression of LOX-1 in primary cultures of human umbilical vein endothelial cells (HUVECs). After treatment with Ang II for 3 hours (1 nmol/L to 1 micromol/L), LOX-1 mRNA was concentration-dependently induced (from 6.9+/-1.4 to 23.1+/-5.5 relative units [RU] by 1 micromol/L Ang II; P<0.05). The angiotensin II type 1 (AT(1)) receptor antagonist losartan prevented this induction. Incubation of HUVECs with Ang II (100 nmol/L, 3 hours) induced LOX-1 protein expression (212+/-21% of control level; P<0. 01) and uptake of 1,1'-dioctadecyl-3,3,3', 3'-tetramethylindocarbocyanine perchlorate (DiI)-labeled oxLDL (209+/-17% of control level; P<0.05) by an AT(1)-dependent pathway, reaching its maximum after 24 hours (680+/-89%; P<0.05). In internal mammary artery biopsy samples from patients with or without ACE inhibitor treatment before coronary artery bypass surgery, LOX-1 mRNA was downregulated by ACE inhibition (6.4+/-2.0 versus 19.3+/-5. 9 RU; n=12 each; P<0.05).
We conclude that LOX-1 is regulated by Ang II in vitro and in vivo, that induction of LOX-1 is mediated by the AT(1) receptor, and that repression of LOX-1 by long-term ACE inhibitor treatment may contribute to the antiatherosclerotic potential of this therapy.</description><subject>Angiotensin II - metabolism</subject><subject>Angiotensin-Converting Enzyme Inhibitors - pharmacology</subject><subject>Anti-Arrhythmia Agents - pharmacology</subject><subject>Antihypertensive Agents - pharmacology</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Cells, Cultured</subject><subject>Coronary Artery Bypass</subject><subject>Coronary Artery Disease - drug therapy</subject><subject>Coronary Artery Disease - metabolism</subject><subject>Coronary Artery Disease - surgery</subject><subject>Down-Regulation - drug effects</subject><subject>Endothelium, Vascular - cytology</subject><subject>Humans</subject><subject>Losartan - pharmacology</subject><subject>Mammary Arteries</subject><subject>Medical sciences</subject><subject>Receptors, LDL - genetics</subject><subject>Receptors, LDL - metabolism</subject><subject>Receptors, Oxidized LDL</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - analysis</subject><subject>Scavenger Receptors, Class E</subject><subject>Umbilical Veins</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkEFr3DAQhUVoaTZp7zkVUUpOtTMjWZZ9DEuTLCwESgO9Ca0kNwpeaSvZJOmvr5ZdaOlhGB588-bxCLlAqBFbvAKsjU81AtR93fX9CVmgYE3VCN6_IQsA6CvJGTslZzk_FdlyKd6RU4Sm7QR2C6Kvw08fJxeyD3S1oj7Y2bhM1_c_KvxCp0dHH-etDtQFG4savR5pcsbtppjoUCa-eOt_O0vH-FzZvdH0Ske_i7tUfH14T94Oeszuw3Gfk4ebr9-Xd9X6_na1vF5XRjRyqgzresuFltI2Xcu5cGJTQhrB28EYh-B0Y7lEO8CGM4GOawTNABrecD1Ifk4uD77l76_Z5UltfTZuHHVwcc5KAiAw2RXw03_gU5xTKNkUQya5kGIPwQEyKeac3KB2yW91elUIat-9AlTL1bciQfWqdF9OPh59583W2X8ODmUX4PMR0NnocUg6GJ__cj3KtmX8D1FJi5A</recordid><startdate>19990831</startdate><enddate>19990831</enddate><creator>MORAWIETZ, H</creator><creator>RUECKSCHLOSS, U</creator><creator>NIEMANN, B</creator><creator>DUERRSCHMIDT, N</creator><creator>GALLE, J</creator><creator>HAKIM, K</creator><creator>ZERKOWSKI, H.-R</creator><creator>SAWAMURA, T</creator><creator>HOLTZ, J</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</general><scope>IQODW</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>K9.</scope><scope>NAPCQ</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>19990831</creationdate><title>Angiotensin II induces LOX-1, the human endothelial receptor for oxidized low-density lipoprotein</title><author>MORAWIETZ, H ; RUECKSCHLOSS, U ; NIEMANN, B ; DUERRSCHMIDT, N ; GALLE, J ; HAKIM, K ; ZERKOWSKI, H.-R ; SAWAMURA, T ; HOLTZ, J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c547t-c289d35a77d486335e5b468c536fcce10ea4d371df0b3251e3a10a2004343af73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Angiotensin II - metabolism</topic><topic>Angiotensin-Converting Enzyme Inhibitors - pharmacology</topic><topic>Anti-Arrhythmia Agents - pharmacology</topic><topic>Antihypertensive Agents - pharmacology</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Cells, Cultured</topic><topic>Coronary Artery Bypass</topic><topic>Coronary Artery Disease - drug therapy</topic><topic>Coronary Artery Disease - metabolism</topic><topic>Coronary Artery Disease - surgery</topic><topic>Down-Regulation - drug effects</topic><topic>Endothelium, Vascular - cytology</topic><topic>Humans</topic><topic>Losartan - pharmacology</topic><topic>Mammary Arteries</topic><topic>Medical sciences</topic><topic>Receptors, LDL - genetics</topic><topic>Receptors, LDL - metabolism</topic><topic>Receptors, Oxidized LDL</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - analysis</topic><topic>Scavenger Receptors, Class E</topic><topic>Umbilical Veins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MORAWIETZ, H</creatorcontrib><creatorcontrib>RUECKSCHLOSS, U</creatorcontrib><creatorcontrib>NIEMANN, B</creatorcontrib><creatorcontrib>DUERRSCHMIDT, N</creatorcontrib><creatorcontrib>GALLE, J</creatorcontrib><creatorcontrib>HAKIM, K</creatorcontrib><creatorcontrib>ZERKOWSKI, H.-R</creatorcontrib><creatorcontrib>SAWAMURA, T</creatorcontrib><creatorcontrib>HOLTZ, J</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>MORAWIETZ, H</au><au>RUECKSCHLOSS, U</au><au>NIEMANN, B</au><au>DUERRSCHMIDT, N</au><au>GALLE, J</au><au>HAKIM, K</au><au>ZERKOWSKI, H.-R</au><au>SAWAMURA, T</au><au>HOLTZ, J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Angiotensin II induces LOX-1, the human endothelial receptor for oxidized low-density lipoprotein</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>1999-08-31</date><risdate>1999</risdate><volume>100</volume><issue>9</issue><spage>899</spage><epage>902</epage><pages>899-902</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Oxidatively modified LDL (oxLDL) plays an important role in the development of atherosclerosis. OxLDL effects, eg, foam cell formation, are mediated in part by the classic scavenger receptor, whereas other effects may involve the recently cloned endothelial oxLDL receptor, LOX-1 (lectinlike oxLDL receptor-1), which is distinct from macrophage scavenger receptors. Because the regulation of LOX-1 must still be defined, we investigated whether LOX-1 is regulated by the potentially proatherosclerotic stimulant angiotensin II (Ang II).
Using competitive reverse transcription-polymerase chain reaction (RT-PCR), we quantified mRNA expression of LOX-1 in primary cultures of human umbilical vein endothelial cells (HUVECs). After treatment with Ang II for 3 hours (1 nmol/L to 1 micromol/L), LOX-1 mRNA was concentration-dependently induced (from 6.9+/-1.4 to 23.1+/-5.5 relative units [RU] by 1 micromol/L Ang II; P<0.05). The angiotensin II type 1 (AT(1)) receptor antagonist losartan prevented this induction. Incubation of HUVECs with Ang II (100 nmol/L, 3 hours) induced LOX-1 protein expression (212+/-21% of control level; P<0. 01) and uptake of 1,1'-dioctadecyl-3,3,3', 3'-tetramethylindocarbocyanine perchlorate (DiI)-labeled oxLDL (209+/-17% of control level; P<0.05) by an AT(1)-dependent pathway, reaching its maximum after 24 hours (680+/-89%; P<0.05). In internal mammary artery biopsy samples from patients with or without ACE inhibitor treatment before coronary artery bypass surgery, LOX-1 mRNA was downregulated by ACE inhibition (6.4+/-2.0 versus 19.3+/-5. 9 RU; n=12 each; P<0.05).
We conclude that LOX-1 is regulated by Ang II in vitro and in vivo, that induction of LOX-1 is mediated by the AT(1) receptor, and that repression of LOX-1 by long-term ACE inhibitor treatment may contribute to the antiatherosclerotic potential of this therapy.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>10468518</pmid><doi>10.1161/01.cir.100.9.899</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Circulation (New York, N.Y.), 1999-08, Vol.100 (9), p.899-902 |
| issn | 0009-7322 1524-4539 |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Ovid Autoload |
| subjects | Angiotensin II - metabolism Angiotensin-Converting Enzyme Inhibitors - pharmacology Anti-Arrhythmia Agents - pharmacology Antihypertensive Agents - pharmacology Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cells, Cultured Coronary Artery Bypass Coronary Artery Disease - drug therapy Coronary Artery Disease - metabolism Coronary Artery Disease - surgery Down-Regulation - drug effects Endothelium, Vascular - cytology Humans Losartan - pharmacology Mammary Arteries Medical sciences Receptors, LDL - genetics Receptors, LDL - metabolism Receptors, Oxidized LDL Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - analysis Scavenger Receptors, Class E Umbilical Veins |
| title | Angiotensin II induces LOX-1, the human endothelial receptor for oxidized low-density lipoprotein |
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