SLO2.1/NALCN a sodium signaling complex that regulates uterine activity.
SLO2.1/NALCN a sodium signaling complex that regulates uterine activity.
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DOI:
10.1016/j.isci.2021.103210
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发表时间:
2021-11-19
期刊:
影响因子:
5.8
通讯作者:
Santi CM
中科院分区:
文献类型:
--
作者:
Ferreira JJ;Amazu C;Puga-Molina LC;Ma X;England SK;Santi CM
Depolarization of the myometrial smooth muscle cell (MSMC) resting membrane potential is necessary for the uterus to transition from a quiescent state to a contractile state. The molecular mechanisms involved in this transition are not completely understood. Here, we report that a coupled system between the Na+-activated K+ channel (SLO2.1) and the non-selective Na+ leak channel (NALCN) determines the MSMC membrane potential. Our data indicate that Na+ entering through NALCN acts as an intracellular signaling molecule that activates SLO2.1. Potassium efflux through SLO2.1 hyperpolarizes the membrane. A decrease in SLO2.1/NALCN activity induces membrane depolarization, triggering Ca2+ entry through voltage-dependent Ca2+ channels and promoting contraction. Consistent with functional coupling, our data show that NALCN and SLO2.1 are in close proximity in human MSMCs. We propose that these arrangements of SLO2.1 and NALCN permit these channels to functionally regulate MSMC membrane potential and cell excitability and modulate uterine contractility. The SLO2.1/NALCN complex controls uterine excitability. A decrease in SLO2.1/NALCN activity triggers uterine contractility. Biological sciences; Cellular physiology; Cell biology; Functional aspects of cell biology
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影响因子:
3.4
作者:
LACAMPAGNE, A;GANNIER, F;LEGUENNEC, JY
通讯作者:
LEGUENNEC, JY
DOI:
10.1098/rspb.1993.0002
发表时间:
1993-01-22
影响因子:
4.7
作者:
KHAN, RN;SMITH, SK;ASHFORD, MLJ
通讯作者:
ASHFORD, MLJ
影响因子:
5.5
作者:
KURIYAMA, H;SUZUKI, H
通讯作者:
SUZUKI, H
影响因子:
25
作者:
Budelli, Gonzalo;Hage, Travis A.;Wei, Aguan;Rojas, Patricio;Jong, Yuh-Jiin Ivy;O'Malley, Karen;Salkoff, Lawrence
通讯作者:
Salkoff, Lawrence
影响因子:
5.5
作者:
AMEDEE, T;MIRONNEAU, C;MIRONNEAU, J
通讯作者:
MIRONNEAU, J