{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T15:29:31Z","timestamp":1790782171947,"version":"4.1.0"},"reference-count":54,"publisher":"Portland Press Ltd.","issue":"4","content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2014,2,1]]},"abstract":"<jats:p>AngII (angiotensin II) is a potent neurohormone responsible for cardiac hypertrophy, in which TGF (transforming growth factor)-\u03b2 serves as a principal downstream mediator. We recently found that ablation of fibulin-2\u00a0in mice attenuated TGF-\u03b2 signalling, protected mice against progressive ventricular dysfunction, and significantly reduced the mortality after experimental MI (myocardial infarction). In the present study, we investigated the role of fibulin-2\u00a0in AngII-induced TGF-\u03b2 signalling and subsequent cardiac hypertrophy. We performed chronic subcutaneous infusion of AngII in fibulin-2 null (Fbln2\u2212\/\u2212), heterozygous (Fbln2+\/\u2212) and WT (wild-type) mice by a mini-osmotic pump. After 4\u00a0weeks of subpressor dosage of AngII infusion (0.2\u00a0\u03bcg\/kg of body weight per min), WT mice developed significant hypertrophy, whereas the Fbln2\u2212\/\u2212 showed no response. In WT, AngII treatment significantly up-regulated mRNAs for fibulin-2, ANP (atrial natriuretic peptide), TGF-\u03b21, Col I (collagen type\u00a0I), Col III (collagen type\u00a0III), MMP (matrix metalloproteinase)-2 and MMP-9, and increased the phosphorylation of TGF-\u03b2-downstream signalling markers, Smad2, TAK1 (TGF-\u03b2-activated kinase 1) and p38 MAPK (mitogen-activated protein kinase), which were all unchanged in AngII-treated Fbln2\u2212\/\u2212 mice. The Fbln2+\/\u2212 mice consistently displayed AngII-induced effects intermediate between WT and Fbln2\u2212\/\u2212. Pressor dosage of AngII (2\u00a0mg\/kg of body weight per min) induced significant fibrosis in WT but not in Fbln2\u2212\/\u2212 mice with comparable hypertension and hypertrophy in both groups. Isolated CFs (cardiac fibroblasts) were treated with AngII, in which direct AngII effects and TGF-\u03b2-mediated autocrine effects was observed in WT. The latter effects were totally abolished in Fbln2\u2212\/\u2212 cells, suggesting that fibulin-2 is essential for AngII-induced TGF-\u03b2 activation. In conclusion our data indicate that fibulin-2 is essential for AngII-induced TGF-\u03b2-mediated cardiac hypertrophy via enhanced TGF-\u03b2 activation and suggest that fibulin-2 is a potential therapeutic target to inhibit AngII-induced cardiac remodelling.<\/jats:p>","DOI":"10.1042\/cs20120636","type":"journal-article","created":{"date-parts":[[2013,7,23]],"date-time":"2013-07-23T18:19:41Z","timestamp":1374603581000},"page":"275-288","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":62,"title":["Fibulin-2 deficiency attenuates angiotensin II-induced cardiac hypertrophy by reducing transforming growth factor-\u03b2 signalling"],"prefix":"10.1042","volume":"126","author":[{"given":"Hangxiang","family":"Zhang","sequence":"first","affiliation":[{"name":"Nemours Biomedical Research and Nemours Cardiac Center, Nemours\/Alfred I. duPont Hospital for Children, Wilmington, DE 19803, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Wu","sequence":"additional","affiliation":[{"name":"Nemours Biomedical Research and Nemours Cardiac Center, Nemours\/Alfred I. duPont Hospital for Children, Wilmington, DE 19803, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hailong","family":"Dong","sequence":"additional","affiliation":[{"name":"Nemours Biomedical Research and Nemours Cardiac Center, Nemours\/Alfred I. duPont Hospital for Children, Wilmington, DE 19803, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shaukat\u00a0A.","family":"Khan","sequence":"additional","affiliation":[{"name":"Nemours Biomedical Research and Nemours Cardiac Center, Nemours\/Alfred I. duPont Hospital for Children, Wilmington, DE 19803, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mon-Li","family":"Chu","sequence":"additional","affiliation":[{"name":"Department of Dermatology and Cutaneous Biology, Thomas Jefferson University, Philadelphia, PA 19107, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takeshi","family":"Tsuda","sequence":"additional","affiliation":[{"name":"Nemours Biomedical Research and Nemours Cardiac Center, Nemours\/Alfred I. duPont Hospital for Children, Wilmington, DE 19803, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2013,10,14]]},"reference":[{"key":"2021113010302269200_B1","doi-asserted-by":"crossref","first-page":"467","DOI":"10.1038\/nm0504-467","article-title":"A decade of discoveries in cardiac biology","volume":"10","author":"Olson","year":"2004","journal-title":"Nat. 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