Figure 1. β1AR stimulation elicits cardiomyocyte death via a RAGE-dependent mechanism.

(A) ISO-induced increase in PI-positive cells was blocked by the βAR blocker Prop. (B) ISO-induced increase in PI-positive cells was abolished by a RAGE decoy, sRAGE. Adult rat cardiomyocytes were subjected to ISO (1 μM) plus a β2AR selective antagonist, ICI (0.1 μM), in the presence or absence of HMGB1 (200 ng/ml), Prop (0.1 μM), or sRAGE (14 ng/ml). Cell death was assessed by PI-positive staining. Data were expressed as mean ± SEM for 4 independent experiments (at least 500 cells from 4 rats for each group); **P < 0.01 versus all of the other groups (A) or versus control and ISO + sRAGE (B), 1-way ANOVA. β1AR, β1-adrenergic receptor; RAGE, receptor for advanced glycation end-products; ISO, isoproterenol; PI, propidium iodide; Prop, propranolol; ICI, ICI 118,551; sRAGE, soluble RAGE; HMGB1, high-mobility group box 1 protein.