{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T13:05:18Z","timestamp":1776258318730,"version":"3.50.1"},"reference-count":45,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2012,8,9]],"date-time":"2012-08-09T00:00:00Z","timestamp":1344470400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2012,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Autoantibodies against the second extracellular loop of \u03b2<jats:sub>1<\/jats:sub>\u2010adrenergic receptor (\u03b2<jats:sub>1<\/jats:sub>\u2010AA) not only contribute to increased susceptibility to heart failure, but also play a causative role in myocardial remodeling through their catecholamine\u2010like effects via binding with the \u03b2<jats:sub>1<\/jats:sub>\u2010adrenergic receptor. The current study was designed to determine whether \u03b2<jats:sub>1<\/jats:sub>\u2010AA isolated from the sera of heart failure patients could cause TNF\u2010\u03b1 secretion from the murine macrophage\u2010like cell line RAW264.7. Blood samples were collected from 40 patients who had suffered heart failure, as well as from 40 healthy subjects. The titer of \u03b2<jats:sub>1<\/jats:sub>\u2010AA and the level of TNF\u2010\u03b1 were detected using ELISA. The effect of \u03b2<jats:sub>1<\/jats:sub>\u2010AA on murine macrophage\u2010like cell line RAW264.7 proliferation was detected by CCK\u20108 kits and CFSE assay. Western blot assay was used to analyze the expression of phospho\u2010VASP. \u03b2<jats:sub>1<\/jats:sub>\u2010AA appeared more frequently in patients with heart failure than in healthy subjects. The \u03b2<jats:sub>1<\/jats:sub>\u2010AA isolated from heart failure patients promoted an increase of TNF\u2010\u03b1 levels, which could be completely blocked by the selective \u03b2<jats:sub>1<\/jats:sub>\u2010adrenergic receptor antagonist metoprolol and the second extracellular loop of \u03b2<jats:sub>1<\/jats:sub>\u2010adrenergic receptor (\u03b2<jats:sub>1<\/jats:sub>\u2010AR\u2010EC<jats:sub>II<\/jats:sub>), but only partially inhibited by PKA inhibitor H89. Furthermore, the \u03b2<jats:sub>1<\/jats:sub>\u2010AA could enhance the proliferation of RAW264.7 cells in vitro. Meanwhile, the expression of phospho\u2010VASP was markedly increased in the presence of \u03b2<jats:sub>1<\/jats:sub>\u2010AA. These results demonstrate for the first time that the \u03b2<jats:sub>1<\/jats:sub>\u2010AA isolated from heart failure patients could bind with \u03b2<jats:sub>1<\/jats:sub>\u2010AR on the surface of RAW264.7 cells, causing the release of TNF\u2010\u03b1 largely in a PKA\u2010dependent fashion. J. Cell. Biochem. 113: 3218\u20133228, 2012. \u00a9 2012 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/jcb.24198","type":"journal-article","created":{"date-parts":[[2012,5,24]],"date-time":"2012-05-24T20:04:46Z","timestamp":1337889886000},"page":"3218-3228","source":"Crossref","is-referenced-by-count":16,"title":["\u03b2<sub>1<\/sub>\u2010adrenergic receptor autoantibodies from heart failure patients enhanced TNF\u2010\u03b1 secretion in RAW264.7 macrophages in a largely PKA\u2010dependent 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