Selective activation of adrenergic β1 receptors induces heme oxygenase 1 production in RAW264.7 cells

We hypothesized that catecholamines through P-adrenoceptor might modulate macrophage function. We showed that isoproterenol concentration-dependently induced HO-1 production through PI-but not beta(2)-adrenoceptor. Production was increased by forskolin and inhibited by pretreatment with the PKA inhibitor, H-89. Furthermore, induction of HO-1 by isoproterenol effectively protected RAW264.7 cells from effects of glucose oxidase treatment, which was abrogated either by HO- inhibitor, ZnPP IX and beta-adenoceptor antagonist, propranolol. Thus, stimulation of HO-1 production through beta(1)-adenoceptors, and via the PKA pathways by isoproterenol, can enable RAW264.7 cells to resist oxidant stress, suggesting that catecholamine hormones may be necessary, at least, to maximize defending role of macrophages. (c) 2005 Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies.