SLO2.1/NALCN a sodium signaling complex that regulates uterine activity

Summary: 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 s...

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Autores principales:	Juan J. Ferreira, Chinwendu Amazu, Lis C. Puga-Molina, Xiaofeng Ma, Sarah K. England, Celia M. Santi
Formato:	article
Lenguaje:	EN
Publicado:	Elsevier 2021
Materias:	Biological sciences Cellular physiology Cell biology Functional aspects of cell biology Science Q
Acceso en línea:	https://doaj.org/article/7110ec77e6cd4632b93850830151803b
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spelling	oai:doaj.org-article:7110ec77e6cd4632b93850830151803b2021-11-20T05:08:19ZSLO2.1/NALCN a sodium signaling complex that regulates uterine activity2589-004210.1016/j.isci.2021.103210https://doaj.org/article/7110ec77e6cd4632b93850830151803b2021-11-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S2589004221011780https://doaj.org/toc/2589-0042Summary: 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.Juan J. FerreiraChinwendu AmazuLis C. Puga-MolinaXiaofeng MaSarah K. EnglandCelia M. SantiElsevierarticleBiological sciencesCellular physiologyCell biologyFunctional aspects of cell biologyScienceQENiScience, Vol 24, Iss 11, Pp 103210- (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Biological sciences Cellular physiology Cell biology Functional aspects of cell biology Science Q
spellingShingle	Biological sciences Cellular physiology Cell biology Functional aspects of cell biology Science Q Juan J. Ferreira Chinwendu Amazu Lis C. Puga-Molina Xiaofeng Ma Sarah K. England Celia M. Santi SLO2.1/NALCN a sodium signaling complex that regulates uterine activity
description	Summary: 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.
format	article
author	Juan J. Ferreira Chinwendu Amazu Lis C. Puga-Molina Xiaofeng Ma Sarah K. England Celia M. Santi
author_facet	Juan J. Ferreira Chinwendu Amazu Lis C. Puga-Molina Xiaofeng Ma Sarah K. England Celia M. Santi
author_sort	Juan J. Ferreira
title	SLO2.1/NALCN a sodium signaling complex that regulates uterine activity
title_short	SLO2.1/NALCN a sodium signaling complex that regulates uterine activity
title_full	SLO2.1/NALCN a sodium signaling complex that regulates uterine activity
title_fullStr	SLO2.1/NALCN a sodium signaling complex that regulates uterine activity
title_full_unstemmed	SLO2.1/NALCN a sodium signaling complex that regulates uterine activity
title_sort	slo2.1/nalcn a sodium signaling complex that regulates uterine activity
publisher	Elsevier
publishDate	2021
url	https://doaj.org/article/7110ec77e6cd4632b93850830151803b
work_keys_str_mv	AT juanjferreira slo21nalcnasodiumsignalingcomplexthatregulatesuterineactivity AT chinwenduamazu slo21nalcnasodiumsignalingcomplexthatregulatesuterineactivity AT liscpugamolina slo21nalcnasodiumsignalingcomplexthatregulatesuterineactivity AT xiaofengma slo21nalcnasodiumsignalingcomplexthatregulatesuterineactivity AT sarahkengland slo21nalcnasodiumsignalingcomplexthatregulatesuterineactivity AT celiamsanti slo21nalcnasodiumsignalingcomplexthatregulatesuterineactivity
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SLO2.1/NALCN a sodium signaling complex that regulates uterine activity

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