{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T15:27:03Z","timestamp":1791300423294,"version":"4.1.0"},"reference-count":45,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2013,4]]},"abstract":"<jats:sec>\n            <jats:title>Objective\u2014<\/jats:title>\n            <jats:p>We aimed to determine the effect of mechanistic target of rapamycin inhibitor everolimus on abdominal aortic aneurysm within the angiotensin II (A2)-infused apolipoprotein E\u2013deficient mouse model.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results\u2014<\/jats:title>\n            <jats:p>Abdominal aortic aneurysm was induced via subcutaneous infusion of A2. Flow cytometry demonstrated increased circulating and aortic C-C chemokine receptor 2 (CCR2) monocytes during A2 infusion. The number of CCR2 monocytes present within the aorta was positively correlated with suprarenal aortic diameter. Simultaneous infusion of everolimus via a second subcutaneous osmotic micropump inhibited A2-induced aortic dilatation. Using flow cytometry and Western blot analysis, decreased aortic dilatation was associated with reduced development of CCR2 bone marrow monocytes, fewer numbers of circulating CCR2 monocytes, and lower aortic CCR2 concentration. In vitro, everolimus inhibited A2-stimulated production of interferon (IFN)-\u03b3 and IFN\u03b3-induced CCR2 expression in apolipoprotein E\u2013deficient mouse bone marrow monocytes. Further, everolimus diminished IFN\u03b3\/lipopolysaccharide-stimulated M1 polarization in apolipoprotein E\u2013deficient mouse bone marrow monocyte\u2013differentiated macrophages.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions\u2014<\/jats:title>\n            <jats:p>Systemic administration of everolimus limits aortic aneurysm in the A2-infused apolipoprotein E\u2013deficient mouse model via suppressed development of bone marrow CCR2 monocytes and reduced egress of these cells into the circulation.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/atvbaha.112.301006","type":"journal-article","created":{"date-parts":[[2013,2,8]],"date-time":"2013-02-08T09:00:21Z","timestamp":1360314021000},"page":"814-821","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":54,"title":["Everolimus Limits Aortic Aneurysm in the Apolipoprotein E\u2013Deficient Mouse by Downregulating C-C Chemokine Receptor 2 Positive Monocytes"],"prefix":"10.1161","volume":"33","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, James Cook University, Townsville, Queensland, Australia (C.S.M., R.J.J., J.V.M., C.R., J.G.); Comparative Genomics Centre, School of Pharmacy and Molecular Sciences, James Cook University, Townsville, Queensland, Australia (A.R., H.K.); School of Surgery, University of Western Australia, Fremantle Hospital, Fremantle. Western Australia, Australia (P.E.N.); School of..."}],"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, James Cook University, Townsville, Queensland, Australia (C.S.M., R.J.J., J.V.M., C.R., J.G.); Comparative Genomics Centre, School of Pharmacy and Molecular Sciences, James Cook University, Townsville, Queensland, Australia (A.R., H.K.); School of Surgery, University of Western Australia, Fremantle Hospital, Fremantle. Western Australia, Australia (P.E.N.); School of..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joseph V.","family":"Moxon","sequence":"additional","affiliation":[{"name":"From the Vascular Biology Unit, Queensland Research Centre for Peripheral Vascular Disease, School of Medicine &amp; Dentistry, James Cook University, Townsville, Queensland, Australia (C.S.M., R.J.J., J.V.M., C.R., J.G.); Comparative Genomics Centre, School of Pharmacy and Molecular Sciences, James Cook University, Townsville, Queensland, Australia (A.R., H.K.); School of Surgery, University of Western Australia, Fremantle Hospital, Fremantle. Western Australia, Australia (P.E.N.); School of..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alicia","family":"Roomberg","sequence":"additional","affiliation":[{"name":"From the Vascular Biology Unit, Queensland Research Centre for Peripheral Vascular Disease, School of Medicine &amp; Dentistry, James Cook University, Townsville, Queensland, Australia (C.S.M., R.J.J., J.V.M., C.R., J.G.); Comparative Genomics Centre, School of Pharmacy and Molecular Sciences, James Cook University, Townsville, Queensland, Australia (A.R., H.K.); School of Surgery, University of Western Australia, Fremantle Hospital, Fremantle. 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Western Australia, Australia (P.E.N.); School of..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catherine","family":"Rush","sequence":"additional","affiliation":[{"name":"From the Vascular Biology Unit, Queensland Research Centre for Peripheral Vascular Disease, School of Medicine &amp; Dentistry, James Cook University, Townsville, Queensland, Australia (C.S.M., R.J.J., J.V.M., C.R., J.G.); Comparative Genomics Centre, School of Pharmacy and Molecular Sciences, James Cook University, Townsville, Queensland, Australia (A.R., H.K.); School of Surgery, University of Western Australia, Fremantle Hospital, Fremantle. 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