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Authordc.contributor.authorCopaja Soto, Miguel 
Authordc.contributor.authorValenzuela, Rodrigo es_CL
Authordc.contributor.authorSaldaña, Adiela es_CL
Authordc.contributor.authorOcaranza, María Paz es_CL
Authordc.contributor.authorJalil Milad, Jorge es_CL
Authordc.contributor.authorVio, Carlos es_CL
Authordc.contributor.authorLijnen, Paul es_CL
Authordc.contributor.authorOrdenes, Gamaliel es_CL
Authordc.contributor.authorVivar Sánchez, Raúl es_CL
Authordc.contributor.authorLavandero González, Sergioes_CL
Authordc.contributor.authorDíaz Araya, Guillermo es_CL
Admission datedc.date.accessioned2010-01-14T14:19:03Z
Available datedc.date.available2010-01-14T14:19:03Z
Publication datedc.date.issued2008-09
Cita de ítemdc.identifier.citationJOURNAL OF THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM Volume: 9 Issue: 3 Pages: 154-162 Published: SEP 2008en_US
Identifierdc.identifier.issn1470-3203
Identifierdc.identifier.other10.1177/1470320308096408
Identifierdc.identifier.urihttps://repositorio.uchile.cl/handle/2250/128181
Abstractdc.description.abstractIntroduction. Isoproterenol treatment of Brown Norway Lewis rats (high and low plasma angiotersin-I-converting enzyme activity., respectively) results in similar cardiac hypertrophy but higher cardiac fibrosis in Brown Norway rats. 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 beta(1,) 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. 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 Nor-way 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 mu M) were also similar in both strains. Conclusion. We conclude that the greater cardiac fibrosis in Brown Norway rats treated with isoproterenol correlates with (lie early and higher expression of proinflammatory factors.en_US
Lenguagedc.language.isoenen_US
Publisherdc.publisherSAGE PUBLICATIONS LTDen_US
Keywordsdc.subjectRENIN-ANGIOTENSINen_US
Títulodc.titleEarly expression of monocyte chemoattractant protein-1 correlates with the onset of isoproterenol-induced cardiac fibrosis in rats with distinct angiotensin-converting enzyme polymorphismen_US
Document typedc.typeArtículo de revistaen_US


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