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Authordc.contributor.authorAránguiz Urroz, Pablo Daniel 
Authordc.contributor.authorCanales Urriola, Jimena Andrea es_CL
Authordc.contributor.authorCopaja, Miguel es_CL
Authordc.contributor.authorTroncoso Cotal, Rodrigo es_CL
Authordc.contributor.authorVicencio Bustamante, José Miguel es_CL
Authordc.contributor.authorCarrillo Ballesteros, Constanza Carolina es_CL
Authordc.contributor.authorLara Peñaloza, Hernán es_CL
Authordc.contributor.authorLavandero González, Sergioes_CL
Authordc.contributor.authorDíaz Araya, Guillermo es_CL
Admission datedc.date.accessioned2011-08-08T13:33:56Z
Available datedc.date.available2011-08-08T13:33:56Z
Publication datedc.date.issued2011-01
Cita de ítemdc.identifier.citationBIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE 1812 (1): 23-31es_CL
Identifierdc.identifier.issn0925-4439
Identifierdc.identifier.urihttp://repositorio.uchile.cl/handle/2250/121571
General notedc.descriptionArtículo de publicación ISIes_CL
Abstractdc.description.abstractAutophagy is a physiological degradative process key to cell survival during nutrient deprivation, cell differentiation and development. It plays a major role in the turnover of damaged macromolecules and organelles, and it has been involved in the pathogenesis of different cardiovascular diseases Activation of the adrenergic system is commonly associated with cardiac fibrosis and remodeling, and cardiac fibroblasts are key players in these processes. Whether adrenergic stimulation modulates cardiac fibroblast autophagy remains unexplored. In the present study, we aimed at this question and evaluated the effects of b(2)-adrenergic stimulation upon autophagy. Cultured adult rat cardiac fibroblasts were treated with agonists or antagonists of beta-adrenergic receptors (b-AR), and autophagy was assessed by electron microscopy. GFP-LC3 subcellular distribution, and immunowesternblot of endogenous LC3. The predominant expression of b(2)-ARs was determined and characterized by radioligand binding assays using [(3)H]dihydroalprenolol. Both, isoproterenol and norepinephrine (non-selective b-AR agonists), as well as salbutamol (selective b(2)-AR agonist) increased autophagic flux, and these effects were blocked by propanolol (b-AR antagonist), ICI-118,551 (selective b2-AR antagonist), 3-methyladenine but not by atenolol (selective b(1)-AR antagonist). The increase in autophagy was correlated with an enhanced degradation of collagen, and this effect was abrogated by the inhibition of autophagic flux. Overall, our data suggest that b(2)-adrenergic stimulation triggers autophagy in cardiac fibroblasts, and that this response could contribute to reduce the deleterious effects of high adrenergic stimulation upon cardiac fibrosis.es_CL
Lenguagedc.language.isoenes_CL
Publisherdc.publisherELSEVIER SCIENCE BVes_CL
Keywordsdc.subjectBETA-ADRENERGIC-RECEPTORSes_CL
Títulodc.titleBeta(2)-adrenergic receptor regulates cardiac fibroblast autophagy and collagen degradationes_CL
Document typedc.typeArtículo de revistaes_CL


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