Itsuro Kazama1, Asuka Baba2, Yoshio Maruyama2. 1. Department of Physiology I, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan. Electronic address: kazaitsu@med.tohoku.ac.jp. 2. Department of Physiology I, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.
Abstract
BACKGROUND: Since lymphocytes predominantly express delayed rectifier K(+)-channels (Kv1.3) that trigger lymphocyte activation, statins, which exert immunosuppressive effects, would affect the channel currents. METHODS: Employing the patch-clamp technique in murine thymocytes, we examined the effects of statins on Kv1.3-channel currents and the membrane capacitance (Cm). RESULTS: Pravastatin significantly suppressed the pulse-end currents of the channels. Lovastatin and simvastatin also suppressed the peak currents, significantly decreasing the Cm. CONCLUSIONS: This study demonstrated for the first time that statins inhibit thymocyte Kv1.3-channels. The slow inactivation patterns induced by lovastatin and simvastatin may be associated with their accumulation in the plasma membranes.
BACKGROUND: Since lymphocytes predominantly express delayed rectifier K(+)-channels (Kv1.3) that trigger lymphocyte activation, statins, which exert immunosuppressive effects, would affect the channel currents. METHODS: Employing the patch-clamp technique in murine thymocytes, we examined the effects of statins on Kv1.3-channel currents and the membrane capacitance (Cm). RESULTS:Pravastatin significantly suppressed the pulse-end currents of the channels. Lovastatin and simvastatin also suppressed the peak currents, significantly decreasing the Cm. CONCLUSIONS: This study demonstrated for the first time that statins inhibit thymocyte Kv1.3-channels. The slow inactivation patterns induced by lovastatin and simvastatin may be associated with their accumulation in the plasma membranes.