The effect of catecholamines and adenosine on the induction of morphological alterations and depigmentation of newt iris epithelial cells in vitro

Abstract

Abstract Catecholamines and adenosine have a stimulating effect on the process of dedifferentiation of cultured iris epithelial cells (IECs) from the adult newt Notophthalmus viridescens. Micromolar concentrations of adrenergic ligands such as isoproterenol, norepinephrine, and epineph-rine induced marked morphological alterations culminating in the stellate configuration and depigmentation of IECs. Dopamine at 100 γ M or higher induced the morphological response, while serotonin was ineffective. The morphological change was transient, requiring 80–90 min for maximum induction, and only a fraction of the cells was responsive. The response was blocked by β-adrenergic antagonists, such as propranolol and alprenolol, but not by α-adrenergic blockers. Adenosine at 10 γ M, or higher, also induced morphological alterations of IECs. The effect of adenosine was partially blocked by various adenosine receptor antagonists. The effect of isoproterenol and norepinephrine on the induction of morphological alterations was potentiated by adenosine. The release of melanosomes from IECs was increased in the presence of catecholamines and adenosine. Catecholamines and adenosine at 10 γ, M increased the in-tracellular levels of cAMP of dedifferentiating dorsal irides. The increase in cAMP levels induced by isoproterenol was inhibited by propranolol and the adenosine receptor antagonist 5é-deoxy-5é-methyl thioadenosine (MTA) partially blocked the effect of adenosine. Our results suggest that adrenergic hormones may be coupled to a β-adrenergic adenylate cyclase system. The presence of an adenosine receptor is also suggested by the results. Our data strongly support previous work in which cAMP and substances related to it induced morphological alterations and depigmentation of IECs [27, 28, 30]. It is proposed that catecholamines and adenosine may participate in the regulation of dedifferentiation during the transdifferentiation of IECs into lens cells.