Is LOX-1 K167N Polymorphism Protective for Coronary Artery Disease?
Background: Human lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1, OLR1) has been identified as a cell surface endocytosis receptor for oxidized low-density lipoprotein (oxLDL) on vascular endothelial cells. OxLDLs are avidly ingested by macrophages, resulting in foam cell formation....
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| Veröffentlicht in: | In vivo (Athens) 2009-11, Vol.23 (6), p.969-973 |
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| creator | Kurnaz, Ozlem Aydogan, Hülya Yilmaz Isbir, C Selim Tekeli, Atike Isbir, Turgay |
| description | Background: Human lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1, OLR1) has been identified as a cell surface
endocytosis receptor for oxidized low-density lipoprotein (oxLDL) on vascular endothelial cells. OxLDLs are avidly ingested
by macrophages, resulting in foam cell formation. OxLDLs are also involved in inducing smooth muscle cell migration, proliferation
and transformation. A single nucleotide polymorphism K167N (G501C) of the LOX-1 gene results in an amino acid dimorphism (Lys/Asn)
at residue 167. Replacement of this Lys residue causes reduced binding and internalization of oxLDL. The purpose of this study
was to investigate the effect of the LOX-1 K167N gene polymorphism in Turkish patients with coronary artery disease (CAD).
Materials and Methods: K167N polymorphism were studied in 91 patients with CAD and 72 healthy controls by the PCR-RFLP method.
Results: The frequencies of the KK genotype and the K allele were higher in the CAD group than the controls (p |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_733694320</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>733694320</sourcerecordid><originalsourceid>FETCH-LOGICAL-h239t-4ffb0edac5287b750a2285b80e6e3e200d087e8072686345a3d1e2fc8d90eadb3</originalsourceid><addsrcrecordid>eNo1z0tLw0AUhuFBFFurf0GyEFwF5pLMZSUl3orBdqHQ3TBJTsxI0qkzaaX_3oHW1bt5OHznDE2JUCQVeabO0RTTXKYyJ-sJugrhG2MuMKaXaEJjGM3IFBWLkJTLdUqSN8LFe7Jy_WFwftvZMCQr70aoR7uHpHU-KZx3G-MPydyPEPNoA5gAD9foojV9gJtTZ-jz-emjeE3L5cuimJdpR5ka06xtKwyNqXMqRSVybCiVeSUxcGAQJzVYCpBYUC45y3LDGgK0rWWjMJimYjN0f7y79e5nB2HUgw019L3ZgNsFLRjjKmMUR3l7krtqgEZvvR3icP3_dwR3R9DZr-7XetBhMH0fOdN2T5nmWnHF_gBlC1-2</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>733694320</pqid></control><display><type>article</type><title>Is LOX-1 K167N Polymorphism Protective for Coronary Artery Disease?</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>Kurnaz, Ozlem ; Aydogan, Hülya Yilmaz ; Isbir, C Selim ; Tekeli, Atike ; Isbir, Turgay</creator><creatorcontrib>Kurnaz, Ozlem ; Aydogan, Hülya Yilmaz ; Isbir, C Selim ; Tekeli, Atike ; Isbir, Turgay</creatorcontrib><description>Background: Human lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1, OLR1) has been identified as a cell surface
endocytosis receptor for oxidized low-density lipoprotein (oxLDL) on vascular endothelial cells. OxLDLs are avidly ingested
by macrophages, resulting in foam cell formation. OxLDLs are also involved in inducing smooth muscle cell migration, proliferation
and transformation. A single nucleotide polymorphism K167N (G501C) of the LOX-1 gene results in an amino acid dimorphism (Lys/Asn)
at residue 167. Replacement of this Lys residue causes reduced binding and internalization of oxLDL. The purpose of this study
was to investigate the effect of the LOX-1 K167N gene polymorphism in Turkish patients with coronary artery disease (CAD).
Materials and Methods: K167N polymorphism were studied in 91 patients with CAD and 72 healthy controls by the PCR-RFLP method.
Results: The frequencies of the KK genotype and the K allele were higher in the CAD group than the controls (p<0.05), while
the frequency of the NN genotype was higher in the control group than in the CAD group (p<0.05). It was observed that the
decreased CAD risk in patients who had the N allele was reversed by male sex (OR: 0.400 â0.481) and smoking (OR: 0.400 â0.949).
Although male sex and smoking were lower than other cardiovascular risk factors in patients with the N allele they were higher
than other cardiovascular risk factors in patients with the K allele. Conclusion: Male sex and smoking decrease the protective
effects of the N allele. The adverse effects of the K allele on the CAD risk resulting from the K167N polymorphism appear
to be independent of other cardiovascular risk factors.</description><identifier>ISSN: 0258-851X</identifier><identifier>EISSN: 1791-7549</identifier><identifier>PMID: 20023241</identifier><language>eng</language><publisher>Greece: International Institute of Anticancer Research</publisher><subject>Coronary Artery Disease - epidemiology ; Coronary Artery Disease - genetics ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Humans ; Male ; Middle Aged ; Molecular Epidemiology ; Polymorphism, Restriction Fragment Length ; Polymorphism, Single Nucleotide ; Scavenger Receptors, Class E - genetics ; Scavenger Receptors, Class E - metabolism ; Smoking ; Turkey - epidemiology</subject><ispartof>In vivo (Athens), 2009-11, Vol.23 (6), p.969-973</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20023241$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kurnaz, Ozlem</creatorcontrib><creatorcontrib>Aydogan, Hülya Yilmaz</creatorcontrib><creatorcontrib>Isbir, C Selim</creatorcontrib><creatorcontrib>Tekeli, Atike</creatorcontrib><creatorcontrib>Isbir, Turgay</creatorcontrib><title>Is LOX-1 K167N Polymorphism Protective for Coronary Artery Disease?</title><title>In vivo (Athens)</title><addtitle>In Vivo</addtitle><description>Background: Human lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1, OLR1) has been identified as a cell surface
endocytosis receptor for oxidized low-density lipoprotein (oxLDL) on vascular endothelial cells. OxLDLs are avidly ingested
by macrophages, resulting in foam cell formation. OxLDLs are also involved in inducing smooth muscle cell migration, proliferation
and transformation. A single nucleotide polymorphism K167N (G501C) of the LOX-1 gene results in an amino acid dimorphism (Lys/Asn)
at residue 167. Replacement of this Lys residue causes reduced binding and internalization of oxLDL. The purpose of this study
was to investigate the effect of the LOX-1 K167N gene polymorphism in Turkish patients with coronary artery disease (CAD).
Materials and Methods: K167N polymorphism were studied in 91 patients with CAD and 72 healthy controls by the PCR-RFLP method.
Results: The frequencies of the KK genotype and the K allele were higher in the CAD group than the controls (p<0.05), while
the frequency of the NN genotype was higher in the control group than in the CAD group (p<0.05). It was observed that the
decreased CAD risk in patients who had the N allele was reversed by male sex (OR: 0.400 â0.481) and smoking (OR: 0.400 â0.949).
Although male sex and smoking were lower than other cardiovascular risk factors in patients with the N allele they were higher
than other cardiovascular risk factors in patients with the K allele. Conclusion: Male sex and smoking decrease the protective
effects of the N allele. The adverse effects of the K allele on the CAD risk resulting from the K167N polymorphism appear
to be independent of other cardiovascular risk factors.</description><subject>Coronary Artery Disease - epidemiology</subject><subject>Coronary Artery Disease - genetics</subject><subject>Female</subject><subject>Gene Frequency</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Molecular Epidemiology</subject><subject>Polymorphism, Restriction Fragment Length</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Scavenger Receptors, Class E - genetics</subject><subject>Scavenger Receptors, Class E - metabolism</subject><subject>Smoking</subject><subject>Turkey - epidemiology</subject><issn>0258-851X</issn><issn>1791-7549</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1z0tLw0AUhuFBFFurf0GyEFwF5pLMZSUl3orBdqHQ3TBJTsxI0qkzaaX_3oHW1bt5OHznDE2JUCQVeabO0RTTXKYyJ-sJugrhG2MuMKaXaEJjGM3IFBWLkJTLdUqSN8LFe7Jy_WFwftvZMCQr70aoR7uHpHU-KZx3G-MPydyPEPNoA5gAD9foojV9gJtTZ-jz-emjeE3L5cuimJdpR5ka06xtKwyNqXMqRSVybCiVeSUxcGAQJzVYCpBYUC45y3LDGgK0rWWjMJimYjN0f7y79e5nB2HUgw019L3ZgNsFLRjjKmMUR3l7krtqgEZvvR3icP3_dwR3R9DZr-7XetBhMH0fOdN2T5nmWnHF_gBlC1-2</recordid><startdate>20091101</startdate><enddate>20091101</enddate><creator>Kurnaz, Ozlem</creator><creator>Aydogan, Hülya Yilmaz</creator><creator>Isbir, C Selim</creator><creator>Tekeli, Atike</creator><creator>Isbir, Turgay</creator><general>International Institute of Anticancer Research</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20091101</creationdate><title>Is LOX-1 K167N Polymorphism Protective for Coronary Artery Disease?</title><author>Kurnaz, Ozlem ; Aydogan, Hülya Yilmaz ; Isbir, C Selim ; Tekeli, Atike ; Isbir, Turgay</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h239t-4ffb0edac5287b750a2285b80e6e3e200d087e8072686345a3d1e2fc8d90eadb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Coronary Artery Disease - epidemiology</topic><topic>Coronary Artery Disease - genetics</topic><topic>Female</topic><topic>Gene Frequency</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Molecular Epidemiology</topic><topic>Polymorphism, Restriction Fragment Length</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Scavenger Receptors, Class E - genetics</topic><topic>Scavenger Receptors, Class E - metabolism</topic><topic>Smoking</topic><topic>Turkey - epidemiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kurnaz, Ozlem</creatorcontrib><creatorcontrib>Aydogan, Hülya Yilmaz</creatorcontrib><creatorcontrib>Isbir, C Selim</creatorcontrib><creatorcontrib>Tekeli, Atike</creatorcontrib><creatorcontrib>Isbir, Turgay</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>In vivo (Athens)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kurnaz, Ozlem</au><au>Aydogan, Hülya Yilmaz</au><au>Isbir, C Selim</au><au>Tekeli, Atike</au><au>Isbir, Turgay</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Is LOX-1 K167N Polymorphism Protective for Coronary Artery Disease?</atitle><jtitle>In vivo (Athens)</jtitle><addtitle>In Vivo</addtitle><date>2009-11-01</date><risdate>2009</risdate><volume>23</volume><issue>6</issue><spage>969</spage><epage>973</epage><pages>969-973</pages><issn>0258-851X</issn><eissn>1791-7549</eissn><abstract>Background: Human lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1, OLR1) has been identified as a cell surface
endocytosis receptor for oxidized low-density lipoprotein (oxLDL) on vascular endothelial cells. OxLDLs are avidly ingested
by macrophages, resulting in foam cell formation. OxLDLs are also involved in inducing smooth muscle cell migration, proliferation
and transformation. A single nucleotide polymorphism K167N (G501C) of the LOX-1 gene results in an amino acid dimorphism (Lys/Asn)
at residue 167. Replacement of this Lys residue causes reduced binding and internalization of oxLDL. The purpose of this study
was to investigate the effect of the LOX-1 K167N gene polymorphism in Turkish patients with coronary artery disease (CAD).
Materials and Methods: K167N polymorphism were studied in 91 patients with CAD and 72 healthy controls by the PCR-RFLP method.
Results: The frequencies of the KK genotype and the K allele were higher in the CAD group than the controls (p<0.05), while
the frequency of the NN genotype was higher in the control group than in the CAD group (p<0.05). It was observed that the
decreased CAD risk in patients who had the N allele was reversed by male sex (OR: 0.400 â0.481) and smoking (OR: 0.400 â0.949).
Although male sex and smoking were lower than other cardiovascular risk factors in patients with the N allele they were higher
than other cardiovascular risk factors in patients with the K allele. Conclusion: Male sex and smoking decrease the protective
effects of the N allele. The adverse effects of the K allele on the CAD risk resulting from the K167N polymorphism appear
to be independent of other cardiovascular risk factors.</abstract><cop>Greece</cop><pub>International Institute of Anticancer Research</pub><pmid>20023241</pmid><tpages>5</tpages></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Coronary Artery Disease - epidemiology Coronary Artery Disease - genetics Female Gene Frequency Genetic Predisposition to Disease Genotype Humans Male Middle Aged Molecular Epidemiology Polymorphism, Restriction Fragment Length Polymorphism, Single Nucleotide Scavenger Receptors, Class E - genetics Scavenger Receptors, Class E - metabolism Smoking Turkey - epidemiology |
| title | Is LOX-1 K167N Polymorphism Protective for Coronary Artery Disease? |
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