ArticleMolecular human reproduction2015
Sodium leak channel, non-selective contributes to the leak current in human myometrial smooth muscle cells from pregnant women.
Article in Molecular human reproduction, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Mutation-specific roles of sustained sodium current (IPNAS nexus · 2025Article
- SLO2.1/NALCN Functional Complex Activity in Mouse Myometrial Smooth Muscle Cells During Pregnancy.Journal of cellular physiology · 2025Article
- Biophysical Mechanisms of Vaginal Smooth Muscle Contraction: The Role of the Membrane Potential and Ion Channels.Pathophysiology : the official journal of the International Society for Pathophysiology · 2024Review
- Whole-exome sequencing reveals candidate high-risk susceptibility genes for endometriosis.Human genomics · 2023Article
- Modeling and experimental approaches for elucidating multi-scale uterine smooth muscle electro- and mechano-physiology: A review.Frontiers in physiology · 2022Review
- Article
- Uterine contractions in rodent models and humans.Acta physiologica (Oxford, England) · 2021Review
- A sodium background conductance controls the spiking pattern of mouse adrenal chromaffin cells in situ.The Journal of physiology · 2021Article
- Progesterone and estrogen regulate NALCN expression in human myometrial smooth muscle cells.American journal of physiology. Endocrinology and metabolism · 2020Article
- Sodium channels and transporters in the myometrium.Current opinion in physiology · 2020Article
- Hyponatraemia reversibly affects human myometrial contractility. An in vitro pilot study.PloS one · 2020Article
- Sodium-activated potassium channels moderate excitability in vascular smooth muscle.The Journal of physiology · 2019Article
- Functional expression of CLIFAHDD and IHPRF pathogenic variants of the NALCN channel in neuronal cells reveals both gain- and loss-of-function properties.Scientific reports · 2019Article
- Increased rate of acute caesarean sections in women with epilepsy: results from the Oppland Perinatal Database in Norway.European journal of neurology · 2019Article
- Oxytocin can regulate myometrial smooth muscle excitability by inhibiting the NaThe Journal of physiology · 2019Article
- Na+-Leak Channel, Non-Selective (NALCN) Regulates Myometrial Excitability and Facilitates Successful Parturition.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2018Article
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5 authors at 2 institutions in 1 country.
Funding
Abstract
Uterine contractions are tightly regulated by the electrical activity of myometrial smooth muscle cells (MSMCs). These cells require a depolarizing current to initiate Ca(2+) influx and induce contraction. Cationic leak channels, which permit a steady flow of cations into a cell, are known to cause membrane depolarization in many tissue types. Previously, a Gd(3+)-sensitive, Na(+)-dependent leak current was identified in the rat myometrium, but the presence of such a current in human MSMCs and the specific ion channel conducting this current was unknown. Here, we report the presence of a Na(+)-dependent leak current in human myometrium and demonstrate that the Na(+)-leak channel, NALCN, contributes to this current. We performed whole-cell voltage-clamp on fresh and cultured MSMCs from uterine biopsies of term, non-laboring women and isolated the leak currents by using Ca(2+) and K(+) channel blockers in the bath solution. Ohmic leak currents were identified in freshly isolated and cultured MSMCs with normalized conductances of 14.6 pS/pF and 10.0 pS/pF, respectively. The myometrial leak current was significantly reduced (P < 0.01) by treating cells with 10 μM Gd(3+) or by superfusing the cells with a Na(+)-free extracellular solution. Reverse transcriptase PCR and immunoblot analysis of uterine biopsies from term, non-laboring women revealed NALCN messenger RNA and protein expression in the myometrium. Notably, ∼90% knockdown of NALCN protein expression with lentivirus-delivered shRNA reduced the Gd(3+)-sensitive leak current density by 42% (P < 0.05). Our results reveal that NALCN, in part, generates the leak current in MSMCs and provide the basis for future research assessing NALCN as a potential molecular target for modulating uterine excitability.
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