{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T14:49:19Z","timestamp":1787755759086,"version":"build-2784847793"},"reference-count":44,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2016,5]]},"abstract":"<jats:sec>\n            <jats:title>Objective\u2014<\/jats:title>\n            <jats:p>Abdominal aortic aneurysm (AAA) is an important cause of mortality in older adults. Activity of the local kallikrein\u2013kinin system may be important in cardiovascular disease. The effect of kinin B2 receptor (B2R) agonist and antagonist peptides on experimental AAA was investigated.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results\u2014<\/jats:title>\n            <jats:p>AAA was induced in apolipoprotein E\u2013deficient mice via infusion of angiotensin II (1.0 \u03bcg\/kg per minute SC). B2R agonists or antagonists were given via injection (2 mg\/kg IP) every other day. The B2R agonist (B9772) promoted aortic rupture in response to angiotensin II associated with an increase in neutrophil infiltration of the aorta in comparison to controls. Mice receiving a B2R\/kinin B1 receptor antagonist (B9430) were relatively protected from aortic rupture. Neutrophil depletion abrogated the ability of the B2R agonist to promote aortic rupture. Progression of angiotensin II\u2013induced aortic dilatation was inhibited in mice receiving a B2R antagonist (B9330). Secretion of metalloproteinase-2 and -9, osteoprotegerin, and osteopontin by human AAA explant was reduced in the presence of the B2R antagonist (B9330). B2R agonist and antagonist peptides enhanced and inhibited, respectively, angiotensin II\u2013induced neutrophil activation and aortic smooth muscle cell inflammatory phenotype. The B2R antagonist (B9330; 5 \u03bcg) delivered directly to the aortic wall 1 week post-AAA induction with calcium phosphate in a rat model reduced aneurysm growth associated with downregulation of aortic metalloproteinase-9.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions\u2014<\/jats:title>\n            <jats:p>B2R signaling promotes aortic rupture within a mouse model associated with the ability to stimulate inflammatory phenotypes of neutrophils and vascular smooth muscle cells. B2R antagonism could be a potential therapy for AAA.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/atvbaha.115.306945","type":"journal-article","created":{"date-parts":[[2016,3,11]],"date-time":"2016-03-11T05:04:37Z","timestamp":1457672677000},"page":"898-907","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":25,"title":["Modulation of Kinin B2 Receptor Signaling Controls Aortic Dilatation and Rupture in the Angiotensin II\u2013Infused Apolipoprotein E\u2013Deficient Mouse"],"prefix":"10.1161","volume":"36","author":[{"given":"Corey S.","family":"Moran","sequence":"first","affiliation":[{"name":"From the Vascular Biology Unit, Queensland Research Centre for Peripheral Vascular Disease, School of Medicine &amp; Dentistry (C.S.M., T.D., R.J.J., E.B., J.G.), and Discipline of Biomedicine, College of Public Health, Medical and Veterinary Sciences (C.M.R.), James Cook University, Townsville, Queensland, Australia; Department of Biochemistry, University of Colorado Denver, Aurora (L.G.); School of Surgery, University of Western Australia, Fremantle Hospital, Fremantle, Western Australia,..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catherine M.","family":"Rush","sequence":"additional","affiliation":[{"name":"From the Vascular Biology Unit, Queensland Research Centre for Peripheral Vascular Disease, School of Medicine &amp; Dentistry (C.S.M., T.D., R.J.J., E.B., J.G.), and Discipline of Biomedicine, College of Public Health, Medical and Veterinary Sciences (C.M.R.), James Cook University, Townsville, Queensland, Australia; Department of Biochemistry, University of Colorado Denver, Aurora (L.G.); School of Surgery, University of Western Australia, Fremantle Hospital, Fremantle, Western Australia,..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tammy","family":"Dougan","sequence":"additional","affiliation":[{"name":"From the Vascular Biology Unit, Queensland Research Centre for Peripheral Vascular Disease, School of Medicine &amp; Dentistry (C.S.M., T.D., R.J.J., E.B., J.G.), and Discipline of Biomedicine, College of Public Health, Medical and Veterinary Sciences (C.M.R.), James Cook University, Townsville, Queensland, Australia; Department of Biochemistry, University of Colorado Denver, Aurora (L.G.); School of Surgery, University of Western Australia, Fremantle Hospital, Fremantle, Western Australia,..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roby J.","family":"Jose","sequence":"additional","affiliation":[{"name":"From the Vascular Biology Unit, Queensland Research Centre for Peripheral Vascular Disease, School of Medicine &amp; Dentistry (C.S.M., T.D., R.J.J., E.B., J.G.), and Discipline of Biomedicine, College of Public Health, Medical and Veterinary Sciences (C.M.R.), James Cook University, Townsville, Queensland, Australia; Department of Biochemistry, University of Colorado Denver, Aurora (L.G.); School of Surgery, University of Western Australia, Fremantle Hospital, Fremantle, Western Australia,..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erik","family":"Biros","sequence":"additional","affiliation":[{"name":"From the Vascular Biology Unit, Queensland Research Centre for Peripheral Vascular Disease, School of Medicine &amp; Dentistry (C.S.M., T.D., R.J.J., E.B., J.G.), and Discipline of Biomedicine, College of Public Health, Medical and Veterinary Sciences (C.M.R.), James Cook University, Townsville, Queensland, Australia; Department of Biochemistry, University of Colorado Denver, Aurora (L.G.); School of Surgery, University of Western Australia, Fremantle Hospital, Fremantle, Western Australia,..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul E.","family":"Norman","sequence":"additional","affiliation":[{"name":"From the Vascular Biology Unit, Queensland Research Centre for Peripheral Vascular Disease, School of Medicine &amp; Dentistry (C.S.M., T.D., R.J.J., E.B., J.G.), and Discipline of Biomedicine, College of Public Health, Medical and Veterinary Sciences (C.M.R.), James Cook University, Townsville, Queensland, Australia; Department of Biochemistry, University of Colorado Denver, Aurora (L.G.); School of Surgery, University of Western Australia, Fremantle Hospital, Fremantle, Western Australia,..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lajos","family":"Gera","sequence":"additional","affiliation":[{"name":"From the Vascular Biology Unit, Queensland Research Centre for Peripheral Vascular Disease, School of Medicine &amp; Dentistry (C.S.M., T.D., R.J.J., E.B., J.G.), and Discipline of Biomedicine, College of Public Health, Medical and Veterinary Sciences (C.M.R.), James Cook University, Townsville, Queensland, Australia; Department of Biochemistry, University of Colorado Denver, Aurora (L.G.); School of Surgery, University of Western Australia, Fremantle Hospital, Fremantle, Western 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