{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T16:24:15Z","timestamp":1762100655472},"reference-count":25,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2007,4,13]],"date-time":"2007-04-13T00:00:00Z","timestamp":1176422400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunology"],"published-print":{"date-parts":[[2007,8]]},"abstract":"<jats:p><jats:bold>Summary<\/jats:bold> Complement is a major pro\u2010inflammatory innate immune system whose serum activity correlates with systolic blood pressure in humans. To date, no studies using <jats:italic>in vivo<\/jats:italic> models have directly examined the role of individual complement components in regulating vessel function, hypertension and cardiac hypertrophy. Herein, <jats:italic>in vivo<\/jats:italic> responses to angiotensin (ang) II were characterized in mice deficient in CD59a or C3. CD59a<jats:sup>\u2013\/\u2013<\/jats:sup> mice had slightly but significantly elevated systolic blood pressure (107\u00b72\u2003\u00b1 1\u00b77\u2003mmHg versus 113\u00b78\u2003\u00b1\u20031\u00b731\u2003mmHg, <jats:italic>P<\/jats:italic>\u2003&lt;\u20030\u00b701, for wild\u2010type and CD59a<jats:sup>\u2013\/\u2013<\/jats:sup>, respectively). Aortic rings from CD59a<jats:sup>\u2013\/\u2013<\/jats:sup> mice showed significantly less platelet endothelial cell adhesion molecule\u20101 (PECAM\u20101) expression, with elevated deposition of membrane attack complex. However, acetylcholine\u2010 and sodium nitroprusside\u2010dependent dilatation, plasma nitrate\/nitrite and aortic cyclic guanosine monophosphate levels were unchanged from wild\u2010type. Also, <jats:italic>in vivo<\/jats:italic> infusion with either ang II or noradrenaline caused similar hypertension and vascular hypertrophy to wild\u2010type. Mice deficient in C3 had similar basal blood pressure to wild type and showed no differences in hypertension or hypertrophy responses to <jats:italic>in vivo<\/jats:italic> infusion with ang II. These data indicate that CD59a deficiency is associated with some vascular alterations that may represent early damage occurring as a result of increased complement attack. However, a direct role for CD59a or C3 in modulating development of ang II\u2010dependent hypertension or hypertrophy <jats:italic>in vivo<\/jats:italic> is excluded and we suggest caution in development of complement intervention strategies for hypertension and heart failure.<\/jats:p>","DOI":"10.1111\/j.1365-2567.2007.02598.x","type":"journal-article","created":{"date-parts":[[2007,4,30]],"date-time":"2007-04-30T13:57:26Z","timestamp":1177941446000},"page":"518-528","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["CD59 or C3 are not requred for angiotensin II\u2010dependent hypertension or hypertrophy in mice"],"prefix":"10.1111","volume":"121","author":[{"given":"Barbara","family":"Coles","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ruth","family":"Lewis","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Peter B.","family":"Anning","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jonathan","family":"Morton","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sivasankar","family":"Baalasubramanian","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"B. Paul","family":"Morgan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Valerie B.","family":"O'Donnell","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2007,4,13]]},"reference":[{"key":"e_1_2_7_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.101.15.1767"},{"key":"e_1_2_7_3_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.98.9.839"},{"key":"e_1_2_7_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(97)09032-6"},{"key":"e_1_2_7_5_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM200003233421202"},{"key":"e_1_2_7_6_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.97.20.2007"},{"key":"e_1_2_7_7_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.101.3.252"},{"key":"e_1_2_7_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9343(99)00066-2"},{"key":"e_1_2_7_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0735-1097(98)00136-3"},{"key":"e_1_2_7_10_2","doi-asserted-by":"publisher","DOI":"10.1001\/jama.286.17.2107"},{"key":"e_1_2_7_11_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM200010193431602"},{"key":"e_1_2_7_12_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000164623.41250.28"},{"key":"e_1_2_7_13_2","doi-asserted-by":"publisher","DOI":"10.1093\/intimm\/dxl023"},{"key":"e_1_2_7_14_2","doi-asserted-by":"publisher","DOI":"10.1097\/01.fjc.0000154371.95907.bd"},{"key":"e_1_2_7_15_2","first-page":"345","article-title":"Relationship between serum C3 levels and traditional risk factors for myocardial infarction","volume":"53","author":"Muscari A","year":"1998","journal-title":"Acta Cardiol"},{"key":"e_1_2_7_16_2","first-page":"247","article-title":"[Evaluation of complement component C4 concentration and immunoglobulins IgA, IgG, and IgM in serum of patients with primary essential hypertension]","volume":"103","author":"Tomaszewski M","year":"2000","journal-title":"Pol Arch Med Wewn"},{"key":"e_1_2_7_17_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000182677.89816.38"},{"key":"e_1_2_7_18_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000129540.83284.ca"},{"key":"e_1_2_7_19_2","doi-asserted-by":"publisher","DOI":"10.1159\/000463125"},{"key":"e_1_2_7_20_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V98.2.442"},{"key":"e_1_2_7_21_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.25.11490"},{"key":"e_1_2_7_22_2","first-page":"491","volume-title":"Methods in Nitric Oxide Research.","author":"Schmidt H","year":"1996"},{"key":"e_1_2_7_23_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.173.6.3684"},{"key":"e_1_2_7_24_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.18.11.1790"},{"key":"e_1_2_7_25_2","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.2001.5276"},{"key":"e_1_2_7_26_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000019584.04929.83"}],"container-title":["Immunology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1111%2Fj.1365-2567.2007.02598.x","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/pdf\/10.1111\/j.1365-2567.2007.02598.x","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,13]],"date-time":"2023-10-13T19:50:25Z","timestamp":1697226625000},"score":1,"resource":{"primary":{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/10.1111\/j.1365-2567.2007.02598.x"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2007,4,13]]},"references-count":25,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2007,8]]}},"alternative-id":["10.1111\/j.1365-2567.2007.02598.x"],"URL":"https:\/\/doi.org\/10.1111\/j.1365-2567.2007.02598.x","archive":["Portico"],"relation":{},"ISSN":["0019-2805","1365-2567"],"issn-type":[{"value":"0019-2805","type":"print"},{"value":"1365-2567","type":"electronic"}],"subject":[],"published":{"date-parts":[[2007,4,13]]},"assertion":[{"value":"2007-04-13","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}