Medical Ovarian Cancer Section, Developmental Therapeutics Department, Clinical Pharmacology Branch, Division of Clinical Sciences, National Cancer Institute, National Institutes of Health, Bldg 10, Rm 13N248, Bethesda, MD 20892, U.S.A.
MODULATION OF INTERFERON γ INDUCED INCREASES IN CATHEPSIN B IN THP-1 CELLS BY ADRENERGIC AGONISTS AND ANTAGONISTS
Article first published online: 2 JAN 2013
© The Author(s) Journal compilation © 1998 International Federation for Cell Biology
Cell Biology International
Volume 22, Issue 1, pages 13–20, January 1998
How to Cite
LI, Q. and BEVER, C. T. (1998), MODULATION OF INTERFERON γ INDUCED INCREASES IN CATHEPSIN B IN THP-1 CELLS BY ADRENERGIC AGONISTS AND ANTAGONISTS. Cell Biology International, 22: 13–20. doi: 10.1006/cbir.1997.0209
- Issue published online: 2 JAN 2013
- Article first published online: 2 JAN 2013
- Received July 1997; accepted 4 December 1997
- Cited By
- multiple sclerosis;
- cathepsin B;
- adrenergic regulation;
In order to investigate the possible modulation of macrophage function by the autonomic nervous system, the effect of adrenergic agonists and antagonists on interferon (IFN)-γ-induced increases in cathepsin B (CB) in a macrophage-like cell line was studied. It has been shown previously that IFN-γ induces increased CB activity in phorbol myristate acetate (PMA)-primed THP-1 cells. Isoproterenol (ISO) (10μm), a mixed β-receptor agonist, increased the induction of CB activity in the cells but norepinephrine (10μm) and epinephrine (10μm), the α and β receptor agonists, had little effect. The addition of the mixed α-receptor antagonist phentolamine (10μm) had no effect on ISO induced increases but the mixed β-receptor antagonist propranolol (10μm) and the selective β1-receptor antagonist atenolol produced significant inhibition. These results suggest that the activation of β-receptors could be involved in the induction of CB activity in macrophages and provide a possible mechanism for the regulation of macrophage effector function by the autonomic nervous system. Dibutyryl cAMP (1mm) alone also induced increases in CB in THP-1 cells, and H-89 or HA1004 abrogated the effect of dibutyryl cAMP, suggesting that the effect of ISO on CB could be through the elevation of cAMP and the activation of cAMP-dependent protein kinases.