Key result
Endothelin-1 acts as an essential co-factor for beta2-adrenergic receptor-induced proliferation of human cardiac fibroblasts, acting independently of beta2-AR stimulation.
Endothelin-1 acts as an essential co-factor for beta2-adrenergic receptor-induced proliferation of human cardiac fibroblasts, independent of beta2-AR stimulation.
We previously demonstrated that chronic stimulation of the beta2-adrenergic receptor (beta2-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. ETA-receptor antagonism or protein kinase C inhibition abolished the beta2-AR-induced increase in cell proliferation. RT-PCR and ELISA analysis demonstrated that although CF synthesized and secreted ET-1, this occurred independently of beta2-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 beta2-AR stimulation.
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Turner et al. (2004) studied Cultured human cardiac fibroblasts. ETA-receptor antagonism or protein kinase C inhibition was evaluated on Cell proliferation. Endothelin-1 acts as an essential co-factor for beta2-adrenergic receptor-induced proliferation of human cardiac fibroblasts, acting independently of beta2-AR stimulation.
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