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  • Title: Pro-apoptotic effects of anti-beta1-adrenergic receptor antibodies in cultured rat cardiomyocytes: actions on endoplasmic reticulum and the prosurvival PI3K-Akt pathway.
    Author: Liang CS, Mao W, Liu J.
    Journal: Autoimmunity; 2008 Sep; 41(6):434-41. PubMed ID: 18781469.
    Abstract:
    An anti-beta(1)-adrenergic receptor antibody against the second extracellular receptor loop (beta(1)-EC(II)) has been shown to cause myocyte apoptosis and dilated cardiomyopathy in animals. We report in this review that the anti-beta(1)-EC(II) antibody increases intracellular Ca(++) transients and exerts a direct apoptotic effect in cultured neonatal rat cardiomyocytes. Both Fab and Fc fragments are required for the full expression of the apoptotic effects of the anti-beta(1)-EC(II) antibody. Our studies further suggest that the anti-beta(1)-EC(II)-antibody acts primarily on the cardiac beta(1)-adrenergic receptor and its post-receptor activation of Ca(++)/Calmodulin dependent protein kinase II (CaMKII) and p-38 mitogen-activated protein kinase (MAPK), leading to endoplasmic reticulum stress as evidenced by the increased expressions of GRP78 and CHOP, as well as the increased processing of the initiator procaspase-12. Also, observed with the apoptotic effect of anti-beta(1)-EC(II) antibody is reduced activity of the phosphatidylinositol (PI) 3-kinase/Akt/STAT3 signaling pathway. Our results suggest that agents that block the activation of p38-MAPK/endoplasmic reticulum stress or reverse the suppression of the prosurvival PI3K/Akt/STAT3 pathway may be explored as potential novel therapeutic modalities in the treatment of dilated cardiomyopathy.
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