Increased vascular MMP-9 in mice lacking RNF213: moyamoya disease susceptibility gene
Moyamoya disease (MMD) is a chronic occlusive cerebrovascular disease with unknown etiology. Recent genetic studies have identified RNF213 as an important susceptibility gene for MMD. To evaluate the role of RNF213 in vascular remodeling, RNF213 knockout mice (RNF213−/−) and their wild-type litterma...
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| Veröffentlicht in: | Neuroreport 2014-12, Vol.25 (18), p.1442-1446 |
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| creator | Sonobe, Shinya Fujimura, Miki Niizuma, Kuniyasu Fujimura, Taku Furudate, Sadanori Nishijima, Yasuo Kure, Shigeo Tominaga, Teiji |
| description | Moyamoya disease (MMD) is a chronic occlusive cerebrovascular disease with unknown etiology. Recent genetic studies have identified RNF213 as an important susceptibility gene for MMD. To evaluate the role of RNF213 in vascular remodeling, RNF213 knockout mice (RNF213−/−) and their wild-type littermates (WT) were subjected to common carotid artery ligation to induce vascular hyperplasia. We examined the vascular expression of matrix metalloproteinase (MMP)-9, known to be increased in MMD. MMP-9 expression was significantly higher in RNF213−/− mice than in wild-type mice 1 and 7 days after common carotid artery ligation. The vascular wall was significantly thinner in RNF213−/− mice at 14 days. The increased vascular expression of MMP-9 and subsequent vascular wall thinning in RNF213−/− mice could reflect the early characteristic of MMD, consistent with the recently proposed constrictive remodeling theory. |
| doi_str_mv | 10.1097/WNR.0000000000000289 |
| format | Article |
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Recent genetic studies have identified RNF213 as an important susceptibility gene for MMD. To evaluate the role of RNF213 in vascular remodeling, RNF213 knockout mice (RNF213−/−) and their wild-type littermates (WT) were subjected to common carotid artery ligation to induce vascular hyperplasia. We examined the vascular expression of matrix metalloproteinase (MMP)-9, known to be increased in MMD. MMP-9 expression was significantly higher in RNF213−/− mice than in wild-type mice 1 and 7 days after common carotid artery ligation. The vascular wall was significantly thinner in RNF213−/− mice at 14 days. The increased vascular expression of MMP-9 and subsequent vascular wall thinning in RNF213−/− mice could reflect the early characteristic of MMD, consistent with the recently proposed constrictive remodeling theory.</description><identifier>ISSN: 0959-4965</identifier><identifier>EISSN: 1473-558X</identifier><identifier>DOI: 10.1097/WNR.0000000000000289</identifier><identifier>PMID: 25383461</identifier><language>eng</language><publisher>Hagerstown, MD: Wolters Kluwer Health | Lippincott Williams & Wilkins</publisher><subject>Adenosine Triphosphatases ; Animals ; Arteries - pathology ; Biological and medical sciences ; Disease Models, Animal ; Fundamental and applied biological sciences. Psychology ; Immunohistochemistry ; Matrix Metalloproteinase 9 - metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Moyamoya Disease - enzymology ; Moyamoya Disease - genetics ; Moyamoya Disease - pathology ; Real-Time Polymerase Chain Reaction ; Ubiquitin-Protein Ligases - deficiency ; Ubiquitin-Protein Ligases - genetics ; Vertebrates: nervous system and sense organs</subject><ispartof>Neuroreport, 2014-12, Vol.25 (18), p.1442-1446</ispartof><rights>2014 Wolters Kluwer Health | Lippincott Williams & Wilkins</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4157-bb9d7aa103e28c71e909e81f9a3aea444b462361753470ed10b6bcd1d80e87a3</citedby><cites>FETCH-LOGICAL-c4157-bb9d7aa103e28c71e909e81f9a3aea444b462361753470ed10b6bcd1d80e87a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=28919409$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25383461$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sonobe, Shinya</creatorcontrib><creatorcontrib>Fujimura, Miki</creatorcontrib><creatorcontrib>Niizuma, Kuniyasu</creatorcontrib><creatorcontrib>Fujimura, Taku</creatorcontrib><creatorcontrib>Furudate, Sadanori</creatorcontrib><creatorcontrib>Nishijima, Yasuo</creatorcontrib><creatorcontrib>Kure, Shigeo</creatorcontrib><creatorcontrib>Tominaga, Teiji</creatorcontrib><title>Increased vascular MMP-9 in mice lacking RNF213: moyamoya disease susceptibility gene</title><title>Neuroreport</title><addtitle>Neuroreport</addtitle><description>Moyamoya disease (MMD) is a chronic occlusive cerebrovascular disease with unknown etiology. Recent genetic studies have identified RNF213 as an important susceptibility gene for MMD. To evaluate the role of RNF213 in vascular remodeling, RNF213 knockout mice (RNF213−/−) and their wild-type littermates (WT) were subjected to common carotid artery ligation to induce vascular hyperplasia. We examined the vascular expression of matrix metalloproteinase (MMP)-9, known to be increased in MMD. MMP-9 expression was significantly higher in RNF213−/− mice than in wild-type mice 1 and 7 days after common carotid artery ligation. The vascular wall was significantly thinner in RNF213−/− mice at 14 days. The increased vascular expression of MMP-9 and subsequent vascular wall thinning in RNF213−/− mice could reflect the early characteristic of MMD, consistent with the recently proposed constrictive remodeling theory.</description><subject>Adenosine Triphosphatases</subject><subject>Animals</subject><subject>Arteries - pathology</subject><subject>Biological and medical sciences</subject><subject>Disease Models, Animal</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Immunohistochemistry</subject><subject>Matrix Metalloproteinase 9 - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Moyamoya Disease - enzymology</subject><subject>Moyamoya Disease - genetics</subject><subject>Moyamoya Disease - pathology</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Ubiquitin-Protein Ligases - deficiency</subject><subject>Ubiquitin-Protein Ligases - genetics</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0959-4965</issn><issn>1473-558X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkNFOFDEUhhujkRV8A2N6Y-LNYE_bmbbeGSJKAkgIBO8mZzpnodKZWdoZyb69s7CK8cYmTZPm-_uffoy9AbEPwpkPV6fn--LvJa17xhagjSrK0n5_zhbCla7Qrip32Kucf8yME2Bfsh1ZKqt0BQt2edT7RJip5T8x-yli4icnZ4Xjoedd8MQj-tvQX_Pz00MJ6iPvhjVuNm9D3gR5nrKn1RiaEMO45tfU0x57scSY6fX23GUXh58vDr4Wx9--HB18Oi68htIUTeNagwhCkbTeADnhyMLSoUJCrXWjK6kqMKXSRlALoqka30JrBVmDape9f3x2lYa7ifJYd2GeJUbsaZhyDZU1lQUxf_f_qFTSWv2A6kfUpyHnRMt6lUKHaV2DqDfq61l9_a_6OfZ22zA1HbV_Qr9dz8C7LTCLxrhM2PuQnzjrwGnhnvrvhzhSyrdxuqdU3xDG8eahdxZSFVKABglGFJsro34Bgc6ZWA</recordid><startdate>20141217</startdate><enddate>20141217</enddate><creator>Sonobe, Shinya</creator><creator>Fujimura, Miki</creator><creator>Niizuma, Kuniyasu</creator><creator>Fujimura, Taku</creator><creator>Furudate, Sadanori</creator><creator>Nishijima, Yasuo</creator><creator>Kure, Shigeo</creator><creator>Tominaga, Teiji</creator><general>Wolters Kluwer Health | Lippincott Williams & Wilkins</general><general>Lippincott Williams & Wilkins</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>7X8</scope><scope>7TK</scope></search><sort><creationdate>20141217</creationdate><title>Increased vascular MMP-9 in mice lacking RNF213: moyamoya disease susceptibility gene</title><author>Sonobe, Shinya ; Fujimura, Miki ; Niizuma, Kuniyasu ; Fujimura, Taku ; Furudate, Sadanori ; Nishijima, Yasuo ; Kure, Shigeo ; Tominaga, Teiji</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4157-bb9d7aa103e28c71e909e81f9a3aea444b462361753470ed10b6bcd1d80e87a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Adenosine Triphosphatases</topic><topic>Animals</topic><topic>Arteries - pathology</topic><topic>Biological and medical sciences</topic><topic>Disease Models, Animal</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Immunohistochemistry</topic><topic>Matrix Metalloproteinase 9 - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Moyamoya Disease - enzymology</topic><topic>Moyamoya Disease - genetics</topic><topic>Moyamoya Disease - pathology</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Ubiquitin-Protein Ligases - deficiency</topic><topic>Ubiquitin-Protein Ligases - genetics</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sonobe, Shinya</creatorcontrib><creatorcontrib>Fujimura, Miki</creatorcontrib><creatorcontrib>Niizuma, Kuniyasu</creatorcontrib><creatorcontrib>Fujimura, Taku</creatorcontrib><creatorcontrib>Furudate, Sadanori</creatorcontrib><creatorcontrib>Nishijima, Yasuo</creatorcontrib><creatorcontrib>Kure, Shigeo</creatorcontrib><creatorcontrib>Tominaga, Teiji</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><collection>Neurosciences Abstracts</collection><jtitle>Neuroreport</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sonobe, Shinya</au><au>Fujimura, Miki</au><au>Niizuma, Kuniyasu</au><au>Fujimura, Taku</au><au>Furudate, Sadanori</au><au>Nishijima, Yasuo</au><au>Kure, Shigeo</au><au>Tominaga, Teiji</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased vascular MMP-9 in mice lacking RNF213: moyamoya disease susceptibility gene</atitle><jtitle>Neuroreport</jtitle><addtitle>Neuroreport</addtitle><date>2014-12-17</date><risdate>2014</risdate><volume>25</volume><issue>18</issue><spage>1442</spage><epage>1446</epage><pages>1442-1446</pages><issn>0959-4965</issn><eissn>1473-558X</eissn><abstract>Moyamoya disease (MMD) is a chronic occlusive cerebrovascular disease with unknown etiology. Recent genetic studies have identified RNF213 as an important susceptibility gene for MMD. To evaluate the role of RNF213 in vascular remodeling, RNF213 knockout mice (RNF213−/−) and their wild-type littermates (WT) were subjected to common carotid artery ligation to induce vascular hyperplasia. We examined the vascular expression of matrix metalloproteinase (MMP)-9, known to be increased in MMD. MMP-9 expression was significantly higher in RNF213−/− mice than in wild-type mice 1 and 7 days after common carotid artery ligation. The vascular wall was significantly thinner in RNF213−/− mice at 14 days. The increased vascular expression of MMP-9 and subsequent vascular wall thinning in RNF213−/− mice could reflect the early characteristic of MMD, consistent with the recently proposed constrictive remodeling theory.</abstract><cop>Hagerstown, MD</cop><pub>Wolters Kluwer Health | Lippincott Williams & Wilkins</pub><pmid>25383461</pmid><doi>10.1097/WNR.0000000000000289</doi><tpages>5</tpages></addata></record> |
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| subjects | Adenosine Triphosphatases Animals Arteries - pathology Biological and medical sciences Disease Models, Animal Fundamental and applied biological sciences. Psychology Immunohistochemistry Matrix Metalloproteinase 9 - metabolism Mice Mice, Inbred C57BL Mice, Knockout Moyamoya Disease - enzymology Moyamoya Disease - genetics Moyamoya Disease - pathology Real-Time Polymerase Chain Reaction Ubiquitin-Protein Ligases - deficiency Ubiquitin-Protein Ligases - genetics Vertebrates: nervous system and sense organs |
| title | Increased vascular MMP-9 in mice lacking RNF213: moyamoya disease susceptibility gene |
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