Microarray Analysis Reveals Overexpression of CD163 and HO-1 in Symptomatic Carotid Plaques

OBJECTIVE—We studied by microarray analysis whether symptomatic and asymptomatic carotid plaques from the same patient differ in gene expression and whether the same changes are present in an independent sample set. METHODS AND RESULTS—Carotid plaques from four patients with bilateral high-grade ste...

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Veröffentlicht in:Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2007-01, Vol.27 (1), p.154-160
Hauptverfasser: Ijäs, Petra, Nuotio, Krista, Saksi, Jani, Soinne, Lauri, Saimanen, Eija, Karjalainen-Lindsberg, Marja-Liisa, Salonen, Oili, Sarna, Seppo, Tuimala, Jarno, Kovanen, Petri T, Kaste, Markku, Lindsberg, Perttu J
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container_issue 1
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container_title Arteriosclerosis, thrombosis, and vascular biology
container_volume 27
creator Ijäs, Petra
Nuotio, Krista
Saksi, Jani
Soinne, Lauri
Saimanen, Eija
Karjalainen-Lindsberg, Marja-Liisa
Salonen, Oili
Sarna, Seppo
Tuimala, Jarno
Kovanen, Petri T
Kaste, Markku
Lindsberg, Perttu J
description OBJECTIVE—We studied by microarray analysis whether symptomatic and asymptomatic carotid plaques from the same patient differ in gene expression and whether the same changes are present in an independent sample set. METHODS AND RESULTS—Carotid plaques from four patients with bilateral high-grade stenosis, one being symptomatic and the other asymptomatic, were analyzed on Affymetrix U95Av2 arrays. 33 genes showed >1.5-fold change between symptomatic and asymptomatic plaques in an intraindividual comparison with FDR ranging from 0.28 to 0.40. Three genes involved in iron-heme homeostasis, CD163, HO-1, and transferrin receptor, were further analyzed in 40 independent plaques. HO-1 (fold-change 1.93, 95%CI 1.04 to 3.94, P=0.040) and CD163 (1.58, 1.11 to 2.40, P=0.013) mRNAs were again induced, and also HO-1 protein was overexpressed in symptomatic plaques (4.38, 1.54 to 12.20, P=0.024). The expression of HO-1 and CD163 correlated with tissue iron content but iron itself was not associated with the symptom status. CONCLUSIONS—Symptomatic plaques show overexpression of CD163 and HO-1 both in intraindividual and interindividual comparison. Their expression correlates with iron deposits but asymptomatic and symptomatic plaques from isolated patients do not differ in macroscopic hemorrhages or iron deposits. We suggest that symptomatic plaques show a more pronounced induction of CD163 and HO-1 in response to plaque hemorrhages.
doi_str_mv 10.1161/01.ATV.0000251991.64617.e7
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METHODS AND RESULTS—Carotid plaques from four patients with bilateral high-grade stenosis, one being symptomatic and the other asymptomatic, were analyzed on Affymetrix U95Av2 arrays. 33 genes showed &gt;1.5-fold change between symptomatic and asymptomatic plaques in an intraindividual comparison with FDR ranging from 0.28 to 0.40. Three genes involved in iron-heme homeostasis, CD163, HO-1, and transferrin receptor, were further analyzed in 40 independent plaques. HO-1 (fold-change 1.93, 95%CI 1.04 to 3.94, P=0.040) and CD163 (1.58, 1.11 to 2.40, P=0.013) mRNAs were again induced, and also HO-1 protein was overexpressed in symptomatic plaques (4.38, 1.54 to 12.20, P=0.024). The expression of HO-1 and CD163 correlated with tissue iron content but iron itself was not associated with the symptom status. CONCLUSIONS—Symptomatic plaques show overexpression of CD163 and HO-1 both in intraindividual and interindividual comparison. Their expression correlates with iron deposits but asymptomatic and symptomatic plaques from isolated patients do not differ in macroscopic hemorrhages or iron deposits. We suggest that symptomatic plaques show a more pronounced induction of CD163 and HO-1 in response to plaque hemorrhages.</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/01.ATV.0000251991.64617.e7</identifier><identifier>PMID: 17095719</identifier><identifier>CODEN: ATVBFA</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Aged ; Antigens, CD - genetics ; Antigens, CD - metabolism ; Antigens, Differentiation, Myelomonocytic - genetics ; Antigens, Differentiation, Myelomonocytic - metabolism ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Carotid Stenosis - genetics ; Carotid Stenosis - metabolism ; Carotid Stenosis - physiopathology ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; DNA - genetics ; Female ; Gene Expression Regulation ; Heme - metabolism ; Heme Oxygenase-1 - genetics ; Heme Oxygenase-1 - metabolism ; Hemorrhage ; Humans ; Iron - metabolism ; Male ; Medical sciences ; Middle Aged ; Neurology ; Neurosurgery ; Oligonucleotide Array Sequence Analysis - methods ; Receptors, Cell Surface - genetics ; Receptors, Cell Surface - metabolism ; Receptors, Transferrin - genetics ; Receptors, Transferrin - metabolism ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Skull, brain, vascular surgery ; Surgery (general aspects). Transplantations, organ and tissue grafts. 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METHODS AND RESULTS—Carotid plaques from four patients with bilateral high-grade stenosis, one being symptomatic and the other asymptomatic, were analyzed on Affymetrix U95Av2 arrays. 33 genes showed &gt;1.5-fold change between symptomatic and asymptomatic plaques in an intraindividual comparison with FDR ranging from 0.28 to 0.40. Three genes involved in iron-heme homeostasis, CD163, HO-1, and transferrin receptor, were further analyzed in 40 independent plaques. HO-1 (fold-change 1.93, 95%CI 1.04 to 3.94, P=0.040) and CD163 (1.58, 1.11 to 2.40, P=0.013) mRNAs were again induced, and also HO-1 protein was overexpressed in symptomatic plaques (4.38, 1.54 to 12.20, P=0.024). The expression of HO-1 and CD163 correlated with tissue iron content but iron itself was not associated with the symptom status. CONCLUSIONS—Symptomatic plaques show overexpression of CD163 and HO-1 both in intraindividual and interindividual comparison. Their expression correlates with iron deposits but asymptomatic and symptomatic plaques from isolated patients do not differ in macroscopic hemorrhages or iron deposits. We suggest that symptomatic plaques show a more pronounced induction of CD163 and HO-1 in response to plaque hemorrhages.</description><subject>Aged</subject><subject>Antigens, CD - genetics</subject><subject>Antigens, CD - metabolism</subject><subject>Antigens, Differentiation, Myelomonocytic - genetics</subject><subject>Antigens, Differentiation, Myelomonocytic - metabolism</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>Carotid Stenosis - genetics</subject><subject>Carotid Stenosis - metabolism</subject><subject>Carotid Stenosis - physiopathology</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>DNA - genetics</subject><subject>Female</subject><subject>Gene Expression Regulation</subject><subject>Heme - metabolism</subject><subject>Heme Oxygenase-1 - genetics</subject><subject>Heme Oxygenase-1 - metabolism</subject><subject>Hemorrhage</subject><subject>Humans</subject><subject>Iron - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neurology</subject><subject>Neurosurgery</subject><subject>Oligonucleotide Array Sequence Analysis - methods</subject><subject>Receptors, Cell Surface - genetics</subject><subject>Receptors, Cell Surface - metabolism</subject><subject>Receptors, Transferrin - genetics</subject><subject>Receptors, Transferrin - metabolism</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Skull, brain, vascular surgery</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. 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Vascular system</topic><topic>Carotid Stenosis - genetics</topic><topic>Carotid Stenosis - metabolism</topic><topic>Carotid Stenosis - physiopathology</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>DNA - genetics</topic><topic>Female</topic><topic>Gene Expression Regulation</topic><topic>Heme - metabolism</topic><topic>Heme Oxygenase-1 - genetics</topic><topic>Heme Oxygenase-1 - metabolism</topic><topic>Hemorrhage</topic><topic>Humans</topic><topic>Iron - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Neurology</topic><topic>Neurosurgery</topic><topic>Oligonucleotide Array Sequence Analysis - methods</topic><topic>Receptors, Cell Surface - genetics</topic><topic>Receptors, Cell Surface - metabolism</topic><topic>Receptors, Transferrin - genetics</topic><topic>Receptors, Transferrin - metabolism</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Skull, brain, vascular surgery</topic><topic>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ijäs, Petra</creatorcontrib><creatorcontrib>Nuotio, Krista</creatorcontrib><creatorcontrib>Saksi, Jani</creatorcontrib><creatorcontrib>Soinne, Lauri</creatorcontrib><creatorcontrib>Saimanen, Eija</creatorcontrib><creatorcontrib>Karjalainen-Lindsberg, Marja-Liisa</creatorcontrib><creatorcontrib>Salonen, Oili</creatorcontrib><creatorcontrib>Sarna, Seppo</creatorcontrib><creatorcontrib>Tuimala, Jarno</creatorcontrib><creatorcontrib>Kovanen, Petri T</creatorcontrib><creatorcontrib>Kaste, Markku</creatorcontrib><creatorcontrib>Lindsberg, Perttu 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>MEDLINE - Academic</collection><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ijäs, Petra</au><au>Nuotio, Krista</au><au>Saksi, Jani</au><au>Soinne, Lauri</au><au>Saimanen, Eija</au><au>Karjalainen-Lindsberg, Marja-Liisa</au><au>Salonen, Oili</au><au>Sarna, Seppo</au><au>Tuimala, Jarno</au><au>Kovanen, Petri T</au><au>Kaste, Markku</au><au>Lindsberg, Perttu J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Microarray Analysis Reveals Overexpression of CD163 and HO-1 in Symptomatic Carotid Plaques</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>2007-01</date><risdate>2007</risdate><volume>27</volume><issue>1</issue><spage>154</spage><epage>160</epage><pages>154-160</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><coden>ATVBFA</coden><abstract>OBJECTIVE—We studied by microarray analysis whether symptomatic and asymptomatic carotid plaques from the same patient differ in gene expression and whether the same changes are present in an independent sample set. METHODS AND RESULTS—Carotid plaques from four patients with bilateral high-grade stenosis, one being symptomatic and the other asymptomatic, were analyzed on Affymetrix U95Av2 arrays. 33 genes showed &gt;1.5-fold change between symptomatic and asymptomatic plaques in an intraindividual comparison with FDR ranging from 0.28 to 0.40. Three genes involved in iron-heme homeostasis, CD163, HO-1, and transferrin receptor, were further analyzed in 40 independent plaques. HO-1 (fold-change 1.93, 95%CI 1.04 to 3.94, P=0.040) and CD163 (1.58, 1.11 to 2.40, P=0.013) mRNAs were again induced, and also HO-1 protein was overexpressed in symptomatic plaques (4.38, 1.54 to 12.20, P=0.024). The expression of HO-1 and CD163 correlated with tissue iron content but iron itself was not associated with the symptom status. CONCLUSIONS—Symptomatic plaques show overexpression of CD163 and HO-1 both in intraindividual and interindividual comparison. Their expression correlates with iron deposits but asymptomatic and symptomatic plaques from isolated patients do not differ in macroscopic hemorrhages or iron deposits. We suggest that symptomatic plaques show a more pronounced induction of CD163 and HO-1 in response to plaque hemorrhages.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>17095719</pmid><doi>10.1161/01.ATV.0000251991.64617.e7</doi><tpages>7</tpages></addata></record>
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subjects Aged
Antigens, CD - genetics
Antigens, CD - metabolism
Antigens, Differentiation, Myelomonocytic - genetics
Antigens, Differentiation, Myelomonocytic - metabolism
Atherosclerosis (general aspects, experimental research)
Biological and medical sciences
Blood and lymphatic vessels
Cardiology. Vascular system
Carotid Stenosis - genetics
Carotid Stenosis - metabolism
Carotid Stenosis - physiopathology
Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous
DNA - genetics
Female
Gene Expression Regulation
Heme - metabolism
Heme Oxygenase-1 - genetics
Heme Oxygenase-1 - metabolism
Hemorrhage
Humans
Iron - metabolism
Male
Medical sciences
Middle Aged
Neurology
Neurosurgery
Oligonucleotide Array Sequence Analysis - methods
Receptors, Cell Surface - genetics
Receptors, Cell Surface - metabolism
Receptors, Transferrin - genetics
Receptors, Transferrin - metabolism
RNA, Messenger - genetics
RNA, Messenger - metabolism
Skull, brain, vascular surgery
Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases
Vascular diseases and vascular malformations of the nervous system
title Microarray Analysis Reveals Overexpression of CD163 and HO-1 in Symptomatic Carotid Plaques
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