Silencing of CDC42 inhibits contraction and growth-related functions in prostate stromal cells, which is mimicked by ML141.

Background: Prostate smooth muscle contraction and stromal growth may contribute to lower urinary tract symptoms suggestive of benign prostatic hyperplasia, but are incompletely understood. A role of the monomeric GTPase CDC42 for smooth muscle contraction and proliferation appears possible, but is unknown for the prostate. Here, we silenced CDC42 expression in prostate stromal cells (WPMY-1), and examined contractility, growth-related functions and responses to the presumed CDC42 inhibitor, ML141.

Antagonism of α-adrenoceptors by β-adrenergic agonists: Structure-function relations of different agonists in prostate smooth muscle contraction.

Effects of β-adrenergic agonists on prostate smooth muscle contraction are poorly characterized, although mirabegron is used for treatment of lower urinary tract symptoms. Off-target effects of several β-adrenergic agonists include antagonism of α-adrenoceptors. Proposed, but unconfirmed explanations include phenylethanolamine backbones, found in some β-adrenergic agonists and imparting interaction with catecholamine binding pockets of adrenoceptors.