Downregulation of the Hemoglobin Scavenger Receptor in Individuals With Diabetes and the Hp 2-2 Genotype: Implications for the Response to Intraplaque Hemorrhage and Plaque Vulnerability
In individuals with diabetes mellitus (DM), the haptoglobin (Hp) genotype is a major determinant of susceptibility to myocardial infarction. We have proposed that this is because of DM and Hp genotype-dependent differences in the response to intraplaque hemorrhage. The macrophage hemoglobin scavengi...
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| Veröffentlicht in: | Circulation research 2007-07, Vol.101 (1), p.106-110 |
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| creator | Levy, Andrew P Purushothaman, K Raman Levy, Nina S Purushothaman, Meerarani Strauss, Merav Asleh, Rabea Marsh, Stuart Cohen, Osher Moestrup, Soren K Moller, Holger J Zias, Elias A Benhayon, Daniel Fuster, Valentin Moreno, Pedro R |
| description | In individuals with diabetes mellitus (DM), the haptoglobin (Hp) genotype is a major determinant of susceptibility to myocardial infarction. We have proposed that this is because of DM and Hp genotype-dependent differences in the response to intraplaque hemorrhage. The macrophage hemoglobin scavenging receptor CD163 plays an essential role in the clearance of hemoglobin released from lysed red blood cells after intraplaque hemorrhage. We sought to test the hypothesis that expression of CD163 is DM and Hp genotype-dependent. CD163 was quantified in plaques by immunohistochemistry, on peripheral blood monocytes (PBMs) by FACS, and as soluble CD163 (sCD163) in plasma by ELISA. In DM plaques, despite an increase in macrophage infiltration, CD163 immunoreactivity was lower, resulting in a dramatic reduction in the percentage of macrophages expressing CD163 (27±2% versus 70±2%, P=0.0001). In individuals with DM as compared with individuals without DM, the percentage of PBMs expressing CD163 was reduced (3.7±0.6% versus 7.1±0.9%, P |
| doi_str_mv | 10.1161/CIRCRESAHA.107.149435 |
| format | Article |
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We have proposed that this is because of DM and Hp genotype-dependent differences in the response to intraplaque hemorrhage. The macrophage hemoglobin scavenging receptor CD163 plays an essential role in the clearance of hemoglobin released from lysed red blood cells after intraplaque hemorrhage. We sought to test the hypothesis that expression of CD163 is DM and Hp genotype-dependent. CD163 was quantified in plaques by immunohistochemistry, on peripheral blood monocytes (PBMs) by FACS, and as soluble CD163 (sCD163) in plasma by ELISA. In DM plaques, despite an increase in macrophage infiltration, CD163 immunoreactivity was lower, resulting in a dramatic reduction in the percentage of macrophages expressing CD163 (27±2% versus 70±2%, P=0.0001). In individuals with DM as compared with individuals without DM, the percentage of PBMs expressing CD163 was reduced (3.7±0.6% versus 7.1±0.9%, P<0.002) whereas soluble plasma CD163 was increased (2.6±1.1 μg/mL versus 1.6±0.8 μg/mL, P<0.0005). Among DM individuals, the Hp 2-2 genotype was associated with a decrease in the percentage of PBMs expressing CD163 (2.3±0.5% versus 5.6±1.3%, P=0.01) and an increase in plasma soluble CD163 (3.0±0.2 μg/mL versus 2.3±0.2 μg/mL, P=0.04). Taken together, these results demonstrate an impaired hemoglobin clearance capacity in Hp 2-2 DM individuals and may provide the key insight explaining the increased incidence of myocardial infarction in this population.</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/CIRCRESAHA.107.149435</identifier><identifier>PMID: 17525367</identifier><language>eng</language><publisher>United States: American Heart Association, Inc</publisher><subject>Antigens, CD - biosynthesis ; Antigens, CD - blood ; Antigens, CD - genetics ; Antigens, Differentiation, Myelomonocytic - biosynthesis ; Antigens, Differentiation, Myelomonocytic - blood ; Antigens, Differentiation, Myelomonocytic - genetics ; Diabetes Mellitus - blood ; Diabetes Mellitus - genetics ; Diabetes Mellitus - pathology ; Down-Regulation - genetics ; Genetic Predisposition to Disease - epidemiology ; Genotype ; Haptoglobins - genetics ; Haptoglobins - metabolism ; Hemoglobins - genetics ; Hemoglobins - metabolism ; Hemorrhage - blood ; Hemorrhage - epidemiology ; Hemorrhage - genetics ; Humans ; Incidence ; Macrophages - metabolism ; Myocardial Infarction - blood ; Myocardial Infarction - epidemiology ; Myocardial Infarction - genetics ; Receptors, Cell Surface - biosynthesis ; Receptors, Cell Surface - blood ; Receptors, Cell Surface - genetics ; Receptors, Scavenger - antagonists & inhibitors ; Receptors, Scavenger - blood ; Receptors, Scavenger - genetics</subject><ispartof>Circulation research, 2007-07, Vol.101 (1), p.106-110</ispartof><rights>2007 American Heart Association, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c3425-1d48bf2624affbc5615cd0b320af2942ae96b178424f25e4097a8e63cda995f13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3687,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17525367$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Levy, Andrew P</creatorcontrib><creatorcontrib>Purushothaman, K Raman</creatorcontrib><creatorcontrib>Levy, Nina S</creatorcontrib><creatorcontrib>Purushothaman, Meerarani</creatorcontrib><creatorcontrib>Strauss, Merav</creatorcontrib><creatorcontrib>Asleh, Rabea</creatorcontrib><creatorcontrib>Marsh, Stuart</creatorcontrib><creatorcontrib>Cohen, Osher</creatorcontrib><creatorcontrib>Moestrup, Soren K</creatorcontrib><creatorcontrib>Moller, Holger J</creatorcontrib><creatorcontrib>Zias, Elias A</creatorcontrib><creatorcontrib>Benhayon, Daniel</creatorcontrib><creatorcontrib>Fuster, Valentin</creatorcontrib><creatorcontrib>Moreno, Pedro R</creatorcontrib><title>Downregulation of the Hemoglobin Scavenger Receptor in Individuals With Diabetes and the Hp 2-2 Genotype: Implications for the Response to Intraplaque Hemorrhage and Plaque Vulnerability</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>In individuals with diabetes mellitus (DM), the haptoglobin (Hp) genotype is a major determinant of susceptibility to myocardial infarction. We have proposed that this is because of DM and Hp genotype-dependent differences in the response to intraplaque hemorrhage. The macrophage hemoglobin scavenging receptor CD163 plays an essential role in the clearance of hemoglobin released from lysed red blood cells after intraplaque hemorrhage. We sought to test the hypothesis that expression of CD163 is DM and Hp genotype-dependent. CD163 was quantified in plaques by immunohistochemistry, on peripheral blood monocytes (PBMs) by FACS, and as soluble CD163 (sCD163) in plasma by ELISA. In DM plaques, despite an increase in macrophage infiltration, CD163 immunoreactivity was lower, resulting in a dramatic reduction in the percentage of macrophages expressing CD163 (27±2% versus 70±2%, P=0.0001). In individuals with DM as compared with individuals without DM, the percentage of PBMs expressing CD163 was reduced (3.7±0.6% versus 7.1±0.9%, P<0.002) whereas soluble plasma CD163 was increased (2.6±1.1 μg/mL versus 1.6±0.8 μg/mL, P<0.0005). Among DM individuals, the Hp 2-2 genotype was associated with a decrease in the percentage of PBMs expressing CD163 (2.3±0.5% versus 5.6±1.3%, P=0.01) and an increase in plasma soluble CD163 (3.0±0.2 μg/mL versus 2.3±0.2 μg/mL, P=0.04). Taken together, these results demonstrate an impaired hemoglobin clearance capacity in Hp 2-2 DM individuals and may provide the key insight explaining the increased incidence of myocardial infarction in this population.</description><subject>Antigens, CD - biosynthesis</subject><subject>Antigens, CD - blood</subject><subject>Antigens, CD - genetics</subject><subject>Antigens, Differentiation, Myelomonocytic - biosynthesis</subject><subject>Antigens, Differentiation, Myelomonocytic - blood</subject><subject>Antigens, Differentiation, Myelomonocytic - genetics</subject><subject>Diabetes Mellitus - blood</subject><subject>Diabetes Mellitus - genetics</subject><subject>Diabetes Mellitus - pathology</subject><subject>Down-Regulation - genetics</subject><subject>Genetic Predisposition to Disease - epidemiology</subject><subject>Genotype</subject><subject>Haptoglobins - genetics</subject><subject>Haptoglobins - metabolism</subject><subject>Hemoglobins - genetics</subject><subject>Hemoglobins - metabolism</subject><subject>Hemorrhage - blood</subject><subject>Hemorrhage - epidemiology</subject><subject>Hemorrhage - genetics</subject><subject>Humans</subject><subject>Incidence</subject><subject>Macrophages - metabolism</subject><subject>Myocardial Infarction - blood</subject><subject>Myocardial Infarction - epidemiology</subject><subject>Myocardial Infarction - genetics</subject><subject>Receptors, Cell Surface - biosynthesis</subject><subject>Receptors, Cell Surface - blood</subject><subject>Receptors, Cell Surface - genetics</subject><subject>Receptors, Scavenger - antagonists & inhibitors</subject><subject>Receptors, Scavenger - blood</subject><subject>Receptors, Scavenger - genetics</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1u2zAQhIWiReOmfYQWPPUml7-i1ZvhpLGBAC2c_hwFSlpabGlRIakYfrU8XejIQI49ERzMfrPYybKPBM8JKciX1Wa72l7fLdfLOcFyTnjJmXiVzYigPOdCktfZDGNc5pIxfJG9C-EvxoQzWr7NLogUVLBCzrLHK3foPexGq6JxPXIaxQ7QGvZuZ11tenTXqAfod-DRFhoYovMoqZu-NQ-mHZUN6I-JHboyqoYIAam-nRADojlFN9C7eBzgK9rsB2ua55iAdMKcXFsIQ_oDii4xo1eDVffjtID3ndrBM_DHpP4ebQ9e1caaeHyfvdEpHj6c38vs17frn6t1fvv9ZrNa3uYN41TkpOWLWtOCcqV13YiCiKbFNaNYaVpyqqAsaiIXnHJNBXBcSrWAgjWtKkuhCbvMPk_cwbu0RIjV3oQGrFU9uDFUEsvTPVkyisnYeBeCB10N3uyVP1YEV6fSqpfSkiSrqbQ09-kcMNZ7aF-mzi0lQzkZDs5G8OGfHQ_gqw6Ujd1_4E_ve6kn</recordid><startdate>20070706</startdate><enddate>20070706</enddate><creator>Levy, Andrew P</creator><creator>Purushothaman, K Raman</creator><creator>Levy, Nina S</creator><creator>Purushothaman, Meerarani</creator><creator>Strauss, Merav</creator><creator>Asleh, Rabea</creator><creator>Marsh, Stuart</creator><creator>Cohen, Osher</creator><creator>Moestrup, Soren K</creator><creator>Moller, Holger J</creator><creator>Zias, Elias A</creator><creator>Benhayon, Daniel</creator><creator>Fuster, Valentin</creator><creator>Moreno, Pedro R</creator><general>American Heart Association, Inc</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>7X8</scope></search><sort><creationdate>20070706</creationdate><title>Downregulation of the Hemoglobin Scavenger Receptor in Individuals With Diabetes and the Hp 2-2 Genotype: Implications for the Response to Intraplaque Hemorrhage and Plaque Vulnerability</title><author>Levy, Andrew P ; Purushothaman, K Raman ; Levy, Nina S ; Purushothaman, Meerarani ; Strauss, Merav ; Asleh, Rabea ; Marsh, Stuart ; Cohen, Osher ; Moestrup, Soren K ; Moller, Holger J ; Zias, Elias A ; Benhayon, Daniel ; Fuster, Valentin ; Moreno, Pedro R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3425-1d48bf2624affbc5615cd0b320af2942ae96b178424f25e4097a8e63cda995f13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Antigens, CD - biosynthesis</topic><topic>Antigens, CD - blood</topic><topic>Antigens, CD - genetics</topic><topic>Antigens, Differentiation, Myelomonocytic - biosynthesis</topic><topic>Antigens, Differentiation, Myelomonocytic - blood</topic><topic>Antigens, Differentiation, Myelomonocytic - genetics</topic><topic>Diabetes Mellitus - blood</topic><topic>Diabetes Mellitus - genetics</topic><topic>Diabetes Mellitus - pathology</topic><topic>Down-Regulation - genetics</topic><topic>Genetic Predisposition to Disease - epidemiology</topic><topic>Genotype</topic><topic>Haptoglobins - genetics</topic><topic>Haptoglobins - metabolism</topic><topic>Hemoglobins - genetics</topic><topic>Hemoglobins - metabolism</topic><topic>Hemorrhage - blood</topic><topic>Hemorrhage - epidemiology</topic><topic>Hemorrhage - genetics</topic><topic>Humans</topic><topic>Incidence</topic><topic>Macrophages - metabolism</topic><topic>Myocardial Infarction - blood</topic><topic>Myocardial Infarction - epidemiology</topic><topic>Myocardial Infarction - genetics</topic><topic>Receptors, Cell Surface - biosynthesis</topic><topic>Receptors, Cell Surface - blood</topic><topic>Receptors, Cell Surface - genetics</topic><topic>Receptors, Scavenger - antagonists & inhibitors</topic><topic>Receptors, Scavenger - blood</topic><topic>Receptors, Scavenger - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Levy, Andrew P</creatorcontrib><creatorcontrib>Purushothaman, K Raman</creatorcontrib><creatorcontrib>Levy, Nina S</creatorcontrib><creatorcontrib>Purushothaman, Meerarani</creatorcontrib><creatorcontrib>Strauss, Merav</creatorcontrib><creatorcontrib>Asleh, Rabea</creatorcontrib><creatorcontrib>Marsh, Stuart</creatorcontrib><creatorcontrib>Cohen, Osher</creatorcontrib><creatorcontrib>Moestrup, Soren K</creatorcontrib><creatorcontrib>Moller, Holger J</creatorcontrib><creatorcontrib>Zias, Elias A</creatorcontrib><creatorcontrib>Benhayon, Daniel</creatorcontrib><creatorcontrib>Fuster, Valentin</creatorcontrib><creatorcontrib>Moreno, Pedro R</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Levy, Andrew P</au><au>Purushothaman, K Raman</au><au>Levy, Nina S</au><au>Purushothaman, Meerarani</au><au>Strauss, Merav</au><au>Asleh, Rabea</au><au>Marsh, Stuart</au><au>Cohen, Osher</au><au>Moestrup, Soren K</au><au>Moller, Holger J</au><au>Zias, Elias A</au><au>Benhayon, Daniel</au><au>Fuster, Valentin</au><au>Moreno, Pedro R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Downregulation of the Hemoglobin Scavenger Receptor in Individuals With Diabetes and the Hp 2-2 Genotype: Implications for the Response to Intraplaque Hemorrhage and Plaque Vulnerability</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>2007-07-06</date><risdate>2007</risdate><volume>101</volume><issue>1</issue><spage>106</spage><epage>110</epage><pages>106-110</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><abstract>In individuals with diabetes mellitus (DM), the haptoglobin (Hp) genotype is a major determinant of susceptibility to myocardial infarction. We have proposed that this is because of DM and Hp genotype-dependent differences in the response to intraplaque hemorrhage. The macrophage hemoglobin scavenging receptor CD163 plays an essential role in the clearance of hemoglobin released from lysed red blood cells after intraplaque hemorrhage. We sought to test the hypothesis that expression of CD163 is DM and Hp genotype-dependent. CD163 was quantified in plaques by immunohistochemistry, on peripheral blood monocytes (PBMs) by FACS, and as soluble CD163 (sCD163) in plasma by ELISA. In DM plaques, despite an increase in macrophage infiltration, CD163 immunoreactivity was lower, resulting in a dramatic reduction in the percentage of macrophages expressing CD163 (27±2% versus 70±2%, P=0.0001). In individuals with DM as compared with individuals without DM, the percentage of PBMs expressing CD163 was reduced (3.7±0.6% versus 7.1±0.9%, P<0.002) whereas soluble plasma CD163 was increased (2.6±1.1 μg/mL versus 1.6±0.8 μg/mL, P<0.0005). Among DM individuals, the Hp 2-2 genotype was associated with a decrease in the percentage of PBMs expressing CD163 (2.3±0.5% versus 5.6±1.3%, P=0.01) and an increase in plasma soluble CD163 (3.0±0.2 μg/mL versus 2.3±0.2 μg/mL, P=0.04). Taken together, these results demonstrate an impaired hemoglobin clearance capacity in Hp 2-2 DM individuals and may provide the key insight explaining the increased incidence of myocardial infarction in this population.</abstract><cop>United States</cop><pub>American Heart Association, Inc</pub><pmid>17525367</pmid><doi>10.1161/CIRCRESAHA.107.149435</doi><tpages>5</tpages></addata></record> |
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| ispartof | Circulation research, 2007-07, Vol.101 (1), p.106-110 |
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| subjects | Antigens, CD - biosynthesis Antigens, CD - blood Antigens, CD - genetics Antigens, Differentiation, Myelomonocytic - biosynthesis Antigens, Differentiation, Myelomonocytic - blood Antigens, Differentiation, Myelomonocytic - genetics Diabetes Mellitus - blood Diabetes Mellitus - genetics Diabetes Mellitus - pathology Down-Regulation - genetics Genetic Predisposition to Disease - epidemiology Genotype Haptoglobins - genetics Haptoglobins - metabolism Hemoglobins - genetics Hemoglobins - metabolism Hemorrhage - blood Hemorrhage - epidemiology Hemorrhage - genetics Humans Incidence Macrophages - metabolism Myocardial Infarction - blood Myocardial Infarction - epidemiology Myocardial Infarction - genetics Receptors, Cell Surface - biosynthesis Receptors, Cell Surface - blood Receptors, Cell Surface - genetics Receptors, Scavenger - antagonists & inhibitors Receptors, Scavenger - blood Receptors, Scavenger - genetics |
| title | Downregulation of the Hemoglobin Scavenger Receptor in Individuals With Diabetes and the Hp 2-2 Genotype: Implications for the Response to Intraplaque Hemorrhage and Plaque Vulnerability |
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