Premium
Selective activation of adrenergic β 1 receptors induces heme oxygenase 1 production in RAW264.7 cells
Author(s) -
Sun Jinji,
Kim Sung Jae,
Park Min Kyu,
Kim Hye Jung,
Tsoy Irina,
Kang Young Jin,
Lee Young Soo,
Seo Han Geuk,
Lee Jae Heun,
Chang Ki Churl
Publication year - 2005
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2005.08.080
Subject(s) - forskolin , stimulation , heme oxygenase , receptor , chemistry , isoprenaline , propranolol , heme , endocrinology , medicine , nadph oxidase , antagonist , adrenergic receptor , catecholamine , pharmacology , biochemistry , enzyme , biology
We hypothesized that catecholamines through β‐adrenoceptor might modulate macrophage function. We showed that isoproterenol concentration‐dependently induced HO‐1 production through β 1 ‐but not β 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‐1 inhibitor, ZnPP IX and β‐adenoceptor antagonist, propranolol. Thus, stimulation of HO‐1 production through β 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.