Catecholamines modulate epidermal growth factor-induced prostaglandin E2 production in amnion-like (WISH) cells by means of a cyclic adenosine monophosphate-dependent pathway.

Abstract

The purpose of this study was to test the hypothesis that catecholamines can modulate epidermal growth factor-induced prostaglandin E2 production in amnion-derived cells via a cyclic adenosine monophosphate-dependent pathway. Human amnion-derived WISH cells were used as the model system to study the regulation of prostaglandin E2 production. The concentrations of prostaglandin E2 and cyclic adenosine monophosphate were measured by radioimmunoassay. Statistical significance was determined with the Student t test. Preexposure of WISH cells to either epinephrine, norepinephrine, or dopamine inhibited epidermal growth factor-induced prostaglandin E2 production. In addition, propranolol blocked both the increase in cyclic adenosine monophosphate accumulation and the inhibition of prostaglandin E2 production caused by epinephrine. These results indicate that epidermal growth factor-induced prostaglandin E2 production can be attenuated by preexposure of amnion cells to catecholamines and that the inhibitory effect of catecholamines on epidermal growth factor response may be mediated via a beta-adrenergic receptor--coupled adenylate cyclase.