C57BL/6 NK cell gene complex is crucially involved in vascular remodeling

Abstract Objective NK cells are known to be involved in cardiovascular disease processes. One of these processes, vascular remodeling, may strongly differ between individuals and mouse strains such as the C57BL/6 and BALB/c. Moreover, C57BL/6 and BALB/c mice vary in immune responses and in the compo...

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Veröffentlicht in:Journal of molecular and cellular cardiology 2013-11, Vol.64, p.51-58
Hauptverfasser: de Vries, M.R, Seghers, L, van Bergen, J, Peters, H.A.B, de Jong, R.C.M, Hamming, J.F, Toes, R.E.M, van Hinsbergh, V.W.M, Quax, P.H.A
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container_start_page 51
container_title Journal of molecular and cellular cardiology
container_volume 64
creator de Vries, M.R
Seghers, L
van Bergen, J
Peters, H.A.B
de Jong, R.C.M
Hamming, J.F
Toes, R.E.M
van Hinsbergh, V.W.M
Quax, P.H.A
description Abstract Objective NK cells are known to be involved in cardiovascular disease processes. One of these processes, vascular remodeling, may strongly differ between individuals and mouse strains such as the C57BL/6 and BALB/c. Moreover, C57BL/6 and BALB/c mice vary in immune responses and in the composition of their Natural Killer gene Complex (NKC). Here we study the role of NK cells, and in particular the C57BL/6 NKC in vascular remodeling and intimal hyperplasia formation. Methods and results C57BL/6, BALB/c and CMV1r mice, a BALB/c strain congenic for the C57BL/6 NKC, were used in an injury induced cuff model and a vein graft model. NK cell depleted C57BL/6 mice demonstrated a 43% reduction in intimal hyperplasia after femoral artery cuff placement compared to control C57BL/6 mice ( p < 0.05). Cuff placement and vein grafting resulted in profound intimal hyperplasia in C57BL/6 mice, but also in CMV1r mice, whereas this was significantly less in BALB/c mice. Significant more leukocyte infiltrations and IFN-γ staining were seen in both C57BL/6 and CMV1r vein grafts compared to BALB/c vein grafts. Conclusions These data demonstrate an important role for NK cells in intimal hyperplasia and vascular remodeling. Furthermore, the C57BL/6 NKC in CMV1r mice stimulates vascular remodeling most likely through the activation of (IFN-γ-secreting) NK-cells that modulate the outcome of vascular remodeling.
doi_str_mv 10.1016/j.yjmcc.2013.08.009
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One of these processes, vascular remodeling, may strongly differ between individuals and mouse strains such as the C57BL/6 and BALB/c. Moreover, C57BL/6 and BALB/c mice vary in immune responses and in the composition of their Natural Killer gene Complex (NKC). Here we study the role of NK cells, and in particular the C57BL/6 NKC in vascular remodeling and intimal hyperplasia formation. Methods and results C57BL/6, BALB/c and CMV1r mice, a BALB/c strain congenic for the C57BL/6 NKC, were used in an injury induced cuff model and a vein graft model. NK cell depleted C57BL/6 mice demonstrated a 43% reduction in intimal hyperplasia after femoral artery cuff placement compared to control C57BL/6 mice ( p &lt; 0.05). Cuff placement and vein grafting resulted in profound intimal hyperplasia in C57BL/6 mice, but also in CMV1r mice, whereas this was significantly less in BALB/c mice. Significant more leukocyte infiltrations and IFN-γ staining were seen in both C57BL/6 and CMV1r vein grafts compared to BALB/c vein grafts. Conclusions These data demonstrate an important role for NK cells in intimal hyperplasia and vascular remodeling. Furthermore, the C57BL/6 NKC in CMV1r mice stimulates vascular remodeling most likely through the activation of (IFN-γ-secreting) NK-cells that modulate the outcome of vascular remodeling.</description><identifier>ISSN: 0022-2828</identifier><identifier>EISSN: 1095-8584</identifier><identifier>DOI: 10.1016/j.yjmcc.2013.08.009</identifier><identifier>PMID: 24013026</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Animals ; Arteries - immunology ; Arteries - metabolism ; Arteries - pathology ; Blood Vessels - immunology ; Blood Vessels - metabolism ; Blood Vessels - pathology ; Cardiovascular ; Cardiovascular disease ; Disease Models, Animal ; Gene Expression Regulation ; Hyperplasia ; IFN-γ ; Inflammation - genetics ; Inflammation - immunology ; Intimal hyperplasia ; Killer Cells, Natural - immunology ; Killer Cells, Natural - metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; NK cell gene complex ; NK cells ; Tunica Intima - immunology ; Tunica Intima - metabolism ; Tunica Intima - pathology ; Vascular remodeling ; Veins - immunology ; Veins - metabolism ; Veins - pathology</subject><ispartof>Journal of molecular and cellular cardiology, 2013-11, Vol.64, p.51-58</ispartof><rights>Elsevier Ltd</rights><rights>2013 Elsevier Ltd</rights><rights>2013.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c414t-2bc29ff281076d28fb951503338da50b190e4fbf277e8b2972aeae1955a0ce0e3</citedby><cites>FETCH-LOGICAL-c414t-2bc29ff281076d28fb951503338da50b190e4fbf277e8b2972aeae1955a0ce0e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.yjmcc.2013.08.009$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,782,786,3554,27933,27934,46004</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24013026$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>de Vries, M.R</creatorcontrib><creatorcontrib>Seghers, L</creatorcontrib><creatorcontrib>van Bergen, J</creatorcontrib><creatorcontrib>Peters, H.A.B</creatorcontrib><creatorcontrib>de Jong, R.C.M</creatorcontrib><creatorcontrib>Hamming, J.F</creatorcontrib><creatorcontrib>Toes, R.E.M</creatorcontrib><creatorcontrib>van Hinsbergh, V.W.M</creatorcontrib><creatorcontrib>Quax, P.H.A</creatorcontrib><title>C57BL/6 NK cell gene complex is crucially involved in vascular remodeling</title><title>Journal of molecular and cellular cardiology</title><addtitle>J Mol Cell Cardiol</addtitle><description>Abstract Objective NK cells are known to be involved in cardiovascular disease processes. One of these processes, vascular remodeling, may strongly differ between individuals and mouse strains such as the C57BL/6 and BALB/c. Moreover, C57BL/6 and BALB/c mice vary in immune responses and in the composition of their Natural Killer gene Complex (NKC). Here we study the role of NK cells, and in particular the C57BL/6 NKC in vascular remodeling and intimal hyperplasia formation. Methods and results C57BL/6, BALB/c and CMV1r mice, a BALB/c strain congenic for the C57BL/6 NKC, were used in an injury induced cuff model and a vein graft model. NK cell depleted C57BL/6 mice demonstrated a 43% reduction in intimal hyperplasia after femoral artery cuff placement compared to control C57BL/6 mice ( p &lt; 0.05). Cuff placement and vein grafting resulted in profound intimal hyperplasia in C57BL/6 mice, but also in CMV1r mice, whereas this was significantly less in BALB/c mice. Significant more leukocyte infiltrations and IFN-γ staining were seen in both C57BL/6 and CMV1r vein grafts compared to BALB/c vein grafts. Conclusions These data demonstrate an important role for NK cells in intimal hyperplasia and vascular remodeling. Furthermore, the C57BL/6 NKC in CMV1r mice stimulates vascular remodeling most likely through the activation of (IFN-γ-secreting) NK-cells that modulate the outcome of vascular remodeling.</description><subject>Animals</subject><subject>Arteries - immunology</subject><subject>Arteries - metabolism</subject><subject>Arteries - pathology</subject><subject>Blood Vessels - immunology</subject><subject>Blood Vessels - metabolism</subject><subject>Blood Vessels - pathology</subject><subject>Cardiovascular</subject><subject>Cardiovascular disease</subject><subject>Disease Models, Animal</subject><subject>Gene Expression Regulation</subject><subject>Hyperplasia</subject><subject>IFN-γ</subject><subject>Inflammation - genetics</subject><subject>Inflammation - immunology</subject><subject>Intimal hyperplasia</subject><subject>Killer Cells, Natural - immunology</subject><subject>Killer Cells, Natural - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>NK cell gene complex</subject><subject>NK cells</subject><subject>Tunica Intima - immunology</subject><subject>Tunica Intima - metabolism</subject><subject>Tunica Intima - pathology</subject><subject>Vascular remodeling</subject><subject>Veins - immunology</subject><subject>Veins - metabolism</subject><subject>Veins - pathology</subject><issn>0022-2828</issn><issn>1095-8584</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1u1DAUhS0EokPhCZCQl2ySXv8ksRcg0RE_FSNYAGvLcW4qBycZ7MmIeXscpnTRDSt78R0f3-8S8pJByYDVV0N5GkbnSg5MlKBKAP2IbBjoqlCVko_JBoDzgiuuLsizlAbIhBTiKbngMmeA1xtys62a691VTb98pg5DoLc4IXXzuA_4m_pEXVyctyGcqJ-Oczhily_0aJNbgo004jh3GPx0-5w86W1I-OLuvCQ_Prz_vv1U7L5-vNm-2xVOMnkoeOu47nuuGDR1x1Xf6opVIIRQna2gZRpQ9m3PmwZVy3XDLVpkuqosOAQUl-T1-d19nH8tmA5m9Gn9up1wXpJhUgqtlaxZRsUZdXFOKWJv9tGPNp4MA7M6NIP569CsDg0okw3l1Ku7gqUdsbvP_JOWgTdnAPOYR4_RJOdxctj5iO5gutn_p-Dtg7zLAr2z4SeeMA3zEqds0DCTuAHzbV3jusXcnuu5Fn8A6DeWmw</recordid><startdate>20131101</startdate><enddate>20131101</enddate><creator>de Vries, M.R</creator><creator>Seghers, L</creator><creator>van Bergen, J</creator><creator>Peters, H.A.B</creator><creator>de Jong, R.C.M</creator><creator>Hamming, J.F</creator><creator>Toes, R.E.M</creator><creator>van Hinsbergh, V.W.M</creator><creator>Quax, P.H.A</creator><general>Elsevier Ltd</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>20131101</creationdate><title>C57BL/6 NK cell gene complex is crucially involved in vascular remodeling</title><author>de Vries, M.R ; Seghers, L ; van Bergen, J ; Peters, H.A.B ; de Jong, R.C.M ; Hamming, J.F ; Toes, R.E.M ; van Hinsbergh, V.W.M ; Quax, P.H.A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c414t-2bc29ff281076d28fb951503338da50b190e4fbf277e8b2972aeae1955a0ce0e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Arteries - immunology</topic><topic>Arteries - metabolism</topic><topic>Arteries - pathology</topic><topic>Blood Vessels - immunology</topic><topic>Blood Vessels - metabolism</topic><topic>Blood Vessels - pathology</topic><topic>Cardiovascular</topic><topic>Cardiovascular disease</topic><topic>Disease Models, Animal</topic><topic>Gene Expression Regulation</topic><topic>Hyperplasia</topic><topic>IFN-γ</topic><topic>Inflammation - genetics</topic><topic>Inflammation - immunology</topic><topic>Intimal hyperplasia</topic><topic>Killer Cells, Natural - immunology</topic><topic>Killer Cells, Natural - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>NK cell gene complex</topic><topic>NK cells</topic><topic>Tunica Intima - immunology</topic><topic>Tunica Intima - metabolism</topic><topic>Tunica Intima - pathology</topic><topic>Vascular remodeling</topic><topic>Veins - immunology</topic><topic>Veins - metabolism</topic><topic>Veins - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>de Vries, M.R</creatorcontrib><creatorcontrib>Seghers, L</creatorcontrib><creatorcontrib>van Bergen, J</creatorcontrib><creatorcontrib>Peters, H.A.B</creatorcontrib><creatorcontrib>de Jong, R.C.M</creatorcontrib><creatorcontrib>Hamming, J.F</creatorcontrib><creatorcontrib>Toes, R.E.M</creatorcontrib><creatorcontrib>van Hinsbergh, V.W.M</creatorcontrib><creatorcontrib>Quax, P.H.A</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>Journal of molecular and cellular cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>de Vries, M.R</au><au>Seghers, L</au><au>van Bergen, J</au><au>Peters, H.A.B</au><au>de Jong, R.C.M</au><au>Hamming, J.F</au><au>Toes, R.E.M</au><au>van Hinsbergh, V.W.M</au><au>Quax, P.H.A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>C57BL/6 NK cell gene complex is crucially involved in vascular remodeling</atitle><jtitle>Journal of molecular and cellular cardiology</jtitle><addtitle>J Mol Cell Cardiol</addtitle><date>2013-11-01</date><risdate>2013</risdate><volume>64</volume><spage>51</spage><epage>58</epage><pages>51-58</pages><issn>0022-2828</issn><eissn>1095-8584</eissn><abstract>Abstract Objective NK cells are known to be involved in cardiovascular disease processes. One of these processes, vascular remodeling, may strongly differ between individuals and mouse strains such as the C57BL/6 and BALB/c. Moreover, C57BL/6 and BALB/c mice vary in immune responses and in the composition of their Natural Killer gene Complex (NKC). Here we study the role of NK cells, and in particular the C57BL/6 NKC in vascular remodeling and intimal hyperplasia formation. Methods and results C57BL/6, BALB/c and CMV1r mice, a BALB/c strain congenic for the C57BL/6 NKC, were used in an injury induced cuff model and a vein graft model. NK cell depleted C57BL/6 mice demonstrated a 43% reduction in intimal hyperplasia after femoral artery cuff placement compared to control C57BL/6 mice ( p &lt; 0.05). Cuff placement and vein grafting resulted in profound intimal hyperplasia in C57BL/6 mice, but also in CMV1r mice, whereas this was significantly less in BALB/c mice. Significant more leukocyte infiltrations and IFN-γ staining were seen in both C57BL/6 and CMV1r vein grafts compared to BALB/c vein grafts. Conclusions These data demonstrate an important role for NK cells in intimal hyperplasia and vascular remodeling. Furthermore, the C57BL/6 NKC in CMV1r mice stimulates vascular remodeling most likely through the activation of (IFN-γ-secreting) NK-cells that modulate the outcome of vascular remodeling.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>24013026</pmid><doi>10.1016/j.yjmcc.2013.08.009</doi><tpages>8</tpages></addata></record>
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subjects Animals
Arteries - immunology
Arteries - metabolism
Arteries - pathology
Blood Vessels - immunology
Blood Vessels - metabolism
Blood Vessels - pathology
Cardiovascular
Cardiovascular disease
Disease Models, Animal
Gene Expression Regulation
Hyperplasia
IFN-γ
Inflammation - genetics
Inflammation - immunology
Intimal hyperplasia
Killer Cells, Natural - immunology
Killer Cells, Natural - metabolism
Male
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Knockout
NK cell gene complex
NK cells
Tunica Intima - immunology
Tunica Intima - metabolism
Tunica Intima - pathology
Vascular remodeling
Veins - immunology
Veins - metabolism
Veins - pathology
title C57BL/6 NK cell gene complex is crucially involved in vascular remodeling
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