ArticleReproductive sciences (Thousand Oaks, Calif.)2018
Anoctamin Channels in Human Myometrium: A Novel Target for Tocolysis.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- BMI-Dependent Associations of the Estradiol-Linked Polymorphism rs117585797 of theLife (Basel, Switzerland) · 2026Article
- A pericyte chloride clamp mechanism governs capillary control of cerebral blood flow.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- TMEM16A Maintains Acrosomal Integrity Through ERK1/2, RhoA, and Actin Cytoskeleton During Capacitation.International journal of molecular sciences · 2025Article
- Human Chorionic Gonadotropin Modulates the Transcriptome of the Myometrium and Cervix in Late Gestation.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
- Anoctamin 1 antagonism potentiates conventional tocolytic-mediated relaxation of pregnant human uterine smooth muscle.The journal of physiological sciences : JPS · 2021Article
- Calcium-Activated Chloride Channels in Myometrial and Vascular Smooth Muscle.Frontiers in physiology · 2021Review
- Extracellular Matrix Rigidity Modulates Human Cervical Smooth Muscle Contractility-New Insights into Premature Cervical Failure and Spontaneous Preterm Birth.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
- Microelectrode array analysis of mouse uterine smooth muscle electrical activity†.Biology of reproduction · 2020Article
- Agonism of the TMEM16A calcium-activated chloride channel modulates airway smooth muscle tone.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Functional comparison of anoctamin 1 antagonists on human uterine smooth muscle contractility and excitability.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
backgroundSpontaneous preterm labor leading to preterm birth is a significant obstetric problem leading to neonatal morbidity and mortality. Current tocolytics are not completely effective and novel targets may afford a therapeutic benefit.
objectiveTo determine whether the anoctamin (ANO) family, including the calcium-activated chloride channel ANO1, is present in pregnant human uterine smooth muscle (USM) and whether pharmacological and genetic modulation of ANO1 modulates USM contraction.
methodsReverse transcription-polymerase chain reaction (RT-PCR), quantitative RT-PCR, and immunohistochemical staining were done to determine which members of the ANO family are expressed in human USM. Uterine smooth muscle strips were studied in an organ bath to determine whether ANO1 antagonists inhibit oxytocin-induced USM contractions. Anoctamin 1 small interfering RNA (siRNA) knockdown was performed to determine its effect on filamentous-/globular (F/G)-actin ratio, a measurement of actin polymerization's role in promoting smooth muscle contraction.
resultsMessenger RNA (mRNA) encoding all members of the ANO family (except ANO7) are expressed in pregnant USM tissue. Anoctamin 1 mRNA expression was decreased 15.2-fold in pregnant USM compared to nonpregnant. Anoctamin 1 protein is expressed in pregnant human USM tissue. Functional organ bath studies with pregnant human USM tissue demonstrated that the ANO1 antagonist benzbromarone attenuates the force and frequency of oxytocin-induced contractions. In human USM cells, siRNA knockdown of ANO1 decreases F-/G-actin ratios.
conclusionMultiple members of the ANO family, including the calcium-activated chloride channel ANO1, are expressed in human USM. Antagonism of ANO1 by pharmacological inhibition and genetic knockdown leads to an attenuation of contraction in pregnant human USM. Anoctamin 1 is a potentially novel target for tocolysis.
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