Abstract
We previously demonstrated that chronic stimulation of the β 2-adrenergic receptor (β 2-AR) increases proliferation of cultured human cardiac fibroblasts (CF) via an autocrine mechanism. Here, we investigated the role of endothelin-1 (ET-1) in this process. ET A-receptor antagonism or protein kinase C inhibition abolished the β 2-AR-induced increase in cell proliferation. RT-PCR and ELISA analysis demonstrated that although CF synthesized and secreted ET-1, this occurred independently of β 2-AR stimulation. Furthermore, despite activation of the MAP kinase pathway, ET-1 treatment did not stimulate CF proliferation. Therefore, the role of ET-1 in this process is that of an essential co-factor acting independently of β 2-AR stimulation.
Published Version
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