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Adrenocorticotropic hormone activates an outward current in cultured mouse peritoneal macrophages
T Fukushima1, M Ichinose, R Shingai
1Department of Information Science, Faculty of Engineering, Iwate University, 020-8551, Morioka, Japan. t5396009@iwate-u.ac.jp
Insights
Adrenocorticotropic hormone (ACTH) activates calcium-dependent potassium channels in macrophages, modulating their immune function. This discovery offers insights into how hormones influence immune cell activity.
Area of Science:
- Immunology
- Cell Physiology
- Endocrinology
Background:
- Adrenocorticotropic hormone (ACTH) plays a role in the immune response.
- Ion channel activity is crucial for cell function, including immune cells.
Purpose of the Study:
- To investigate the effects of ACTH on ion channel activity in macrophages.
- To determine the specific ion channels modulated by ACTH in immunocompetent cells.
Main Methods:
- Cultured mouse peritoneal macrophages were utilized.
- The perforated patch-clamp technique was employed to analyze ion channel activity.
- Electrophysiological recordings were performed to measure ion currents.
Main Results:
- ACTH induced outward currents in macrophages, dependent on external potassium (K+) concentrations.
- These ACTH-induced currents were blocked by quinine and partially suppressed by tetraethylammonium (TEA).
- The response was dependent on extracellular calcium (Ca2+), indicating a Ca2+-dependent mechanism.
Conclusions:
- ACTH modulates macrophage function by activating calcium-dependent potassium channels.
- This highlights a novel mechanism for hormonal regulation of immune cell activity.
- Findings suggest a link between the endocrine and immune systems at the cellular level.
Abstract:
To define the effects of adrenocorticotropic hormone (ACTH) in immunocompetent cells, ion channel activities in cultured mouse peritoneal macrophages were analyzed by the perforated patch-clamp method. ACTH induced outward currents at smaller holding potentials than K+ equilibrium potentials. Reversal potentials of ACTH-induced currents were dependent on external K+ concentrations, but not on external Cl- concentration. Quinine potently blocked the outward current and tetraethylammonium (TEA) partially suppressed that current. ACTH did not induce the response in Ca2+ free solution containing EGTA. These results suggest that ACTH can modulate macrophage functions through the activation of Ca2+ dependent K+ channels.