Key result
Actin disruption by cytochalasin D prolongs Ca2+-activated Cl- current deactivation by ~54% in murine cells.
Why the study?
The regulation of Ca2+-activated Cl- channel activity by the actin cytoskeleton in murine portal vein smooth muscle cells was examined to understand TMEM16A modulation.
Absolute Event Rate: 85.3% vs 55.3%
p-value: p=<0.05
The study demonstrates that CaCC activity in murine portal vein smooth muscle cells is modulated by the interaction of TMEM16A with the actin cytoskeleton.
Cytoskeletal modulation of CaCC in murine vascular smooth muscle; hypothesis-generating and leaves open in vivo relevance.
TMEM16A is a major component of Ca(2+)-activated Cl(-) channel (CaCC) conductance in murine portal vein smooth muscle cells (mPVSMCs). Here, the regulation of CaCC activity by the actin cytoskeleton was examined in mPVSMCs. Actin disruption by cytochalasin D did not affect the current density, but increased the deactivation time constant in mPVSMCs. The elongated deactivation was recovered by jasplakinolide. When murine TMEM16A was transfected into HEK293 cells that have a poorly developed actin cytoskeleton, electrophysiological properties of CaCC currents were not changed by cytochalasin D. In conclusion, the CaCC activity in mPVSMCs is modified by the interaction of TMEM16A with abundant actin cytoskeleton.
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Ohshiro et al. (2014) studied Basic science (murine portal vein smooth muscle cells). Cytochalasin D vs. Vehicle control (1% DMSO) was evaluated on Time constant of deactivation (tdeact) at +60 mV (p=<0.05). Actin disruption by cytochalasin D significantly elongated the deactivation time constant of Ca2+-activated Cl- currents in murine portal vein smooth muscle cells from 55.3 ms to 85.3 ms.
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