Microtubule-dependent regulation of TMEM16A-mediated Ca2+-activated Cl− currents in vascular smooth muscle cells

Abstract

TMEM16A channels mediate Ca²⁺-activated Cl⁻ (Cl_Ca) currents in vascular smooth muscle cells (VSMCs), and their activity is influenced by cytoskeletal dynamics. The present study examined the functional role of microtubules in TMEM16A regulation. Treatment with microtubule polymerization inhibitors, colchicine and nocodazole, reduced plasma membrane localization of TMEM16A protein and TMEM16A-mediated Cl_Ca currents. Similar effects were observed in TMEM16A-expressing HEK293 cells, with IC₅₀ values of 3.0 μM for colchicine and 0.6 μM for nocodazole. In contrast, acute application had no significant effect. These findings indicate that microtubules are required for maintaining the expression and functional activity of TMEM16A channels in VSMCs.