{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T01:55:53Z","timestamp":1777859753661,"version":"3.51.4"},"reference-count":29,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2008,9,1]],"date-time":"2008-09-01T00:00:00Z","timestamp":1220227200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Renin Angiotensin Aldosterone Syst"],"published-print":{"date-parts":[[2008,9]]},"abstract":"<jats:p>Introduction. Isoproterenol treatment of Brown Norway and Lewis rats (high and low plasma angiotensin-I-converting enzyme activity, respectively) results in similar cardiac hypertrophy but higher cardiac fibrosis in Brown Norway rats.<\/jats:p>\n                  <jats:p>\n                    Materials and methods. Rats were infused in vivo with isoproterenol for two or 10 days. Cardiac fibrosis and inflammation were evaluated histochemically. We measured the mRNAs of pro-fibrotic factors (transforming growth factor \u03b2\n                    <jats:sub>1<\/jats:sub>\n                    , endothelin-1) and pro-inflammatory factors (monocyte chemoattractant protein-1). In studies with cardiac fibroblasts incubated with isoproterenol in vitro , we measured cell proliferation, angiotensin-I-converting enzyme and matrix metalloprotease 2 activities and deposition of collagen type I and fibronectin.\n                  <\/jats:p>\n                  <jats:p>Results. After treatment with isoproterenol for two days, there were large areas of myocardial injury and numerous inflammatory foci in the left ventricle, these being greater in Brown-Norway than in Lewis rats. After treatment with isoproterenol for 10 days, there were large areas of damage with extensive collagen deposition only in the left ventricle; both strains exhibited this damage which was, however, more severe in Brown-Norway than in Lewis rats. After treatment with isoproterenol for two, but not 10, days, greater amounts of monocyte chemoattractant protein-1 mRNA were found in Brown Norway than in Lewis rats. Cell proliferation, activities of angiotensin-I-converting enzyme and matrix metalloprotease 2, amounts of collagen type I and fibronectin were similar in cardiac fibroblasts from both strains; changes after isoproterenol (10 \u00b5M) were also similar in both strains.<\/jats:p>\n                  <jats:p>Conclusion. We conclude that the greater cardiac fibrosis in Brown Norway rats treated with isoproterenol correlates with the early and higher expression of proinflammatory factors.<\/jats:p>","DOI":"10.1177\/1470320308096408","type":"journal-article","created":{"date-parts":[[2008,10,20]],"date-time":"2008-10-20T11:35:16Z","timestamp":1224502516000},"page":"154-162","source":"Crossref","is-referenced-by-count":8,"title":["Early expression of monocyte chemoattractant protein-1 correlates with the onset of isoproterenol-induced cardiac fibrosis in rats with distinct angiotensin-converting enzyme polymorphism"],"prefix":"10.1177","volume":"9","author":[{"given":"Miguel","family":"Copaja Soto","sequence":"first","affiliation":[{"name":"Centro FONDAP Estudios Moleculares de la C\u00e9lula, Universidad de Chile, Santiago, Chile"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rodrigo","family":"Valenzuela","sequence":"additional","affiliation":[{"name":"Centro FONDAP Estudios Moleculares de la C\u00e9lula, Universidad de Chile, Santiago, Chile"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Adiela","family":"Salda\u00f1a","sequence":"additional","affiliation":[{"name":"Centro FONDAP Estudios Moleculares de la C\u00e9lula, Universidad de Chile, Santiago, Chile"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mar\u00eda","family":"Paz Ocaranza","sequence":"additional","affiliation":[{"name":"Departamento Enfermedades Cardiovasculares, Escuela de Medicina, Pontificia Universidad Cat\u00f3lica de Chile, Santiago, Chile"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jorge E.","family":"Jalil","sequence":"additional","affiliation":[{"name":"Departamento Enfermedades Cardiovasculares, Escuela de Medicina, Pontificia Universidad Cat\u00f3lica de Chile, Santiago, Chile"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carlos","family":"Vio","sequence":"additional","affiliation":[{"name":"Facultad de 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Facultad de Medicina, Universidad de Chile, Santiago, Chile"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Guillermo","family":"D\u00edaz-Araya","sequence":"additional","affiliation":[{"name":"Centro FONDAP Estudios Moleculares de la C\u00e9lula, Universidad de Chile, Santiago, Chile,"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2008,9,1]]},"reference":[{"key":"atypb1","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.83.6.1849"},{"key":"atypb2","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.1993.00410080011002"},{"key":"atypb3","doi-asserted-by":"crossref","first-page":"415","DOI":"10.1016\/S0031-6997(24)01458-3","volume":"52","author":"de Gasparo M.","year":"2000","journal-title":"Pharmacol 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