Modulation of TMEM16A-Channel Activity as Ca2+ Activated Cl− Conductance via the Interaction With Actin Cytoskeleton in Murine Portal Vein

Abstract.: TMEM16A is a major component of Ca2+-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...

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Main Authors: Junya Ohshiro, Hisao Yamamura, Yoshiaki Suzuki, Yuji Imaizumi
Format: Article
Language:English
Published: Elsevier 2014-01-01
Series:Journal of Pharmacological Sciences
Online Access:http://www.sciencedirect.com/science/article/pii/S1347861319301586
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spelling doaj-198a282206f147199978e85d5f00ad4a2020-11-24T22:00:36ZengElsevierJournal of Pharmacological Sciences1347-86132014-01-011251107111Modulation of TMEM16A-Channel Activity as Ca2+ Activated Cl− Conductance via the Interaction With Actin Cytoskeleton in Murine Portal VeinJunya Ohshiro0Hisao Yamamura1Yoshiaki Suzuki2Yuji Imaizumi3Department of Molecular and Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya 467-8603, JapanDepartment of Molecular and Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya 467-8603, JapanDepartment of Molecular and Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya 467-8603, JapanDepartment of Molecular and Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya 467-8603, Japan; Corresponding author. yimaizum@phar.nagoya-cu.ac.jpAbstract.: TMEM16A is a major component of Ca2+-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. Keywords:: TMEM16A, actin cytoskeleton, portal veinhttp://www.sciencedirect.com/science/article/pii/S1347861319301586
collection DOAJ
language English
format Article
sources DOAJ
author Junya Ohshiro
Hisao Yamamura
Yoshiaki Suzuki
Yuji Imaizumi
spellingShingle Junya Ohshiro
Hisao Yamamura
Yoshiaki Suzuki
Yuji Imaizumi
Modulation of TMEM16A-Channel Activity as Ca2+ Activated Cl− Conductance via the Interaction With Actin Cytoskeleton in Murine Portal Vein
Journal of Pharmacological Sciences
author_facet Junya Ohshiro
Hisao Yamamura
Yoshiaki Suzuki
Yuji Imaizumi
author_sort Junya Ohshiro
title Modulation of TMEM16A-Channel Activity as Ca2+ Activated Cl− Conductance via the Interaction With Actin Cytoskeleton in Murine Portal Vein
title_short Modulation of TMEM16A-Channel Activity as Ca2+ Activated Cl− Conductance via the Interaction With Actin Cytoskeleton in Murine Portal Vein
title_full Modulation of TMEM16A-Channel Activity as Ca2+ Activated Cl− Conductance via the Interaction With Actin Cytoskeleton in Murine Portal Vein
title_fullStr Modulation of TMEM16A-Channel Activity as Ca2+ Activated Cl− Conductance via the Interaction With Actin Cytoskeleton in Murine Portal Vein
title_full_unstemmed Modulation of TMEM16A-Channel Activity as Ca2+ Activated Cl− Conductance via the Interaction With Actin Cytoskeleton in Murine Portal Vein
title_sort modulation of tmem16a-channel activity as ca2+ activated cl− conductance via the interaction with actin cytoskeleton in murine portal vein
publisher Elsevier
series Journal of Pharmacological Sciences
issn 1347-8613
publishDate 2014-01-01
description Abstract.: TMEM16A is a major component of Ca2+-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. Keywords:: TMEM16A, actin cytoskeleton, portal vein
url http://www.sciencedirect.com/science/article/pii/S1347861319301586
work_keys_str_mv AT junyaohshiro modulationoftmem16achannelactivityasca2activatedclconductanceviatheinteractionwithactincytoskeletoninmurineportalvein
AT hisaoyamamura modulationoftmem16achannelactivityasca2activatedclconductanceviatheinteractionwithactincytoskeletoninmurineportalvein
AT yoshiakisuzuki modulationoftmem16achannelactivityasca2activatedclconductanceviatheinteractionwithactincytoskeletoninmurineportalvein
AT yujiimaizumi modulationoftmem16achannelactivityasca2activatedclconductanceviatheinteractionwithactincytoskeletoninmurineportalvein
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