These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: β1-Adrenoceptor autoantibodies from DCM patients enhance the proliferation of T lymphocytes through the β1-AR/cAMP/PKA and p38 MAPK pathways.
    Author: Du Y, Yan L, Wang J, Zhan W, Song K, Han X, Li X, Cao J, Liu H.
    Journal: PLoS One; 2012; 7(12):e52911. PubMed ID: 23300817.
    Abstract:
    BACKGROUND: Autoantibodies against the second extracellular loop of the β(1)-adrenergic receptor (β(1)-AA) not only contribute to increased susceptibility to heart failure, but also play a causative role in myocardial remodeling through their sympathomimetic-like effects that are induced upon binding to the β(1)-adrenergic receptor. However, their role in the function of T lymphocytes has never been previously investigated. Our present study was designed to determine whether β(1)-AA isolated from the sera of dilated cardiomyopathy (DCM) patients caused the proliferation of T cells and the secretion of cytokines. METHODS: Blood samples were collected from 95 DCM patients as well as 95 healthy subjects, and β(1)-AA was detected using ELISA. The CD3(+)T lymphocytes were selected separately through flow cytometry and the effect of β(1)-AA on T lymphocyte proliferation was examined by CCK-8 kits and CFSE assay. Western blotting was used to analyze the expressions of phospho-VASP and phospho-p38 MAPK. RESULTS: β(1)-AA enhanced the proliferation of T lymphocytes. This effect could be blocked by the selective β(1)-adrenergic receptor antagonist metoprolol, PKA inhibitor H89, and p38 MAPK inhibitor SB203580. Furthermore, the expression of the phosphorylated forms of phospho-VASP and phospho-p38 MAPK were markedly increased in the presence of β(1)-AA. β(1)-AA also inhibited the secretion of interferon-γ (IFN-γ) while promoting an increase in interleukin-4 (IL-4) levels. CONCLUSIONS: These results demonstrate that β(1)-AA isolated from DCM patients binds to β(1)-AR on the surface of T cells, causing changes in T-cell proliferation and secretion through the β(1)-AR/cAMP/PKA and p38 MAPK pathways.
    [Abstract] [Full Text] [Related] [New Search]