Nigerian Journal of Physiological Sciences
Physiological Society of Nigeria
Vol. 25, No. 1, 2010, pp. 5-16
Bioline Code: np10003
Full paper language: English
Document type: Research Article
Document available free of charge
Nigerian Journal of Physiological Sciences, Vol. 25, No. 1, 2010, pp. 5-16
© Copyright 2010 - Physiological Society of Nigeria
Catecholamines Inhibit Gastric Epithelial [RGM-1] Cell Proliferation via Beta Adrenoceptors|
Olaleye , S.B; Wu, W.K.K & Cho , C.H
Catecholamines have been implicated in the modulation of normal cell growth, exerting inhibitory or
excitatory control depending on the cell type. However, there is a dearth of information on the role of adrenergic mediators
in gastric cell proliferation. In the present study, the effects of adrenaline (ADR) and noradrenaline (NOR) on mucosal cell
growth and the cell cycle were evaluated in vitro using a normal rat gastric mucosal cell line RGM-1. Cell proliferation
was assessed using [3H]-thymidine incorporation and cell cycle patterns were determined by DNA labeling with propidium
iodide and flow cytometric quantification. The expressions of adrenoceptors in RGM-1 were determined by Western blot.
ADR (0.01 – 10μM) and NOR (0.01 – 10μM) inhibited the growth of RGM-1 cells in a concentration-dependent manner.
Pre-treatment of cells with ADR and NOR also inhibited the proliferation stimulated by epidermal growth factor (EGF).
Neither phentolamine (non-selective α-adrenergic blocker), methoxamine (α1-selective agonist) nor clonidine (α2-selective
agonist) significantly affected the inhibition of cell proliferation produced by ADR and NOR. Propranolol (non-selective
β-adrenergic blocker) and butoxamine (selective β2-adrenergic blocker) significantly (but not totally) reversed the
inhibitory action of ADR on cell proliferation. Furthermore, procaterol (selective beta-2 agonist) but not dobutamine
(selective beta-1 agonist) had effects similar to those produced by ADR and NOR. Exposure of RGM-1 cells to both ADR
and NOR caused significant inhibition of the G1 – S cycle progression as evidenced by the higher percentage of the G0/G1
phase and a decreased S- phase. This effect was blocked by pre-treatment with propranolol but not phentolamine These
results indicate that catecholamines inhibit the proliferation of RGM-1 cells probably partly through beta-2 receptors.
Cathecholamines; RGM-1; Cell proliferation; cell cycle; flow cytometry, [3H]-thymidine