ArticleThe Journal of physiology2007
Depletion of membrane cholesterol eliminates the Ca2+-activated component of outward potassium current and decreases membrane capacitance in rat uterine myocytes.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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50 citing papers in PubMed, 101 citations in OpenAlex.
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- Piezo1, the new actor in cell volume regulation.Pflugers Archiv : European journal of physiology · 2024Review
- The impact of maternal obesity on in vivo uterine contractile activity during parturition in the rat.Physiological reports · 2023Article
- The Pathophysiology of Labor Dystocia: Theme with Variations.Reproductive sciences (Thousand Oaks, Calif.) · 2023Review
- Cholesterol and PIPAdvances in experimental medicine and biology · 2023Article
- Nanosecond Pulsed Electric Field (nsPEF): Opening the Biotechnological Pandora's Box.International journal of molecular sciences · 2022Review
- Dynein regulates Kv7.4 channel trafficking from the cell membrane.The Journal of general physiology · 2021Article
- The Membrane Cholesterol Modulates the Interaction Between 17-βEstradiol and the BK Channel.Frontiers in pharmacology · 2021Article
- Metabolic Pathways Associated With Term Labor Induction Course in African American Women.Biological research for nursing · 2020Article
- Article
- Preventing Cesarean Birth in Women with Obesity: Influence of Unit-Level Midwifery Presence on Use of Cesarean among Women in the Consortium on Safe Labor Data Set.Journal of midwifery & women's health · 2020Article
- The unique N-terminal sequence of the BKCa channel α-subunit determines its modulation by β-subunits.PloS one · 2017Article
- BKCa channel regulates calcium oscillations induced by alpha-2-macroglobulin in human myometrial smooth muscle cells.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Modelling maternal obesity: the effects of a chronic high-fat, high-cholesterol diet on uterine expression of contractile-associated proteins and ex vivo contractile activity during labour in the rat.Clinical science (London, England : 1979) · 2016Article
- Parturition dysfunction in obesity: time to target the pathobiology.Reproductive biology and endocrinology : RB&E · 2015Review
- Inhibition of CaV2.3 channels by NK1 receptors is sensitive to membrane cholesterol but insensitive to caveolin-1.Pflugers Archiv : European journal of physiology · 2015Article
- Atherosclerosis differentially affects calcium signalling in endothelial cells from aortic arch and thoracic aorta in Apolipoprotein E knockout mice.Physiological reports · 2014Article
- Sarcolemmal cholesterol and caveolin-3 dependence of cardiac function, ischemic tolerance, and opioidergic cardioprotection.American journal of physiology. Heart and circulatory physiology · 2014Article
- Store-operated Ca²⁺ entry and depolarization explain the anomalous behaviour of myometrial SR: effects of SERCA inhibition on electrical activity, Ca²⁺ and force.Cell calcium · 2014Article
- The bestrophin- and TMEM16A-associated Ca(2+)- activated Cl(–) channels in vascular smooth muscles.Channels (Austin, Tex.) · 2014Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Changes in membrane cholesterol content have potent effects on cell signalling and contractility in rat myometrium and other smooth muscles. We have previously shown that depletion of cholesterol with methyl-beta-cyclodextrin (MCD) disrupts caveolar microdomains. The aim of this work was to determine the mechanism underlying the increase in Ca(2+) signalling and contractility occurring in the myometrium with MCD. Patch clamp data obtained on freshly isolated myocytes from the uterus of day 19-21 rats showed that outward K(+) current was significantly reduced by MCD. Membrane capacitance was also reduced. Cholesterol-saturated MCD had no effect on the amplitude of outward current suggesting that the reduction in the outward current was due to cholesterol depletion induced by MCD rather than a direct inhibitory action of MCD on the K(+) channels. Confocal visualization of the membrane bound indicator Calcium Green C18, revealed internalization of the surface membrane with MCD treatment. Large conductance, Ca(2+)-sensitive K(+) channel proteins have been shown to localize to caveolae. When these channels were blocked by iberiotoxin outward current was significantly reduced in the uterine myocytes; MCD treatment reduced the density of outward current. Following reduction of outward current by MCD pretreatment, iberiotoxin was unable to produce any additional decrease in the current, suggesting a common target. MCD treatment also increased the amplitude and frequency of spontaneous rises in cytosolic Ca(2+) level ([Ca(2+)](i) transients) in isolated myocytes. In intact rat myometrium, MCD treatment increased Ca(2+) signalling and contractility, consistent with previous findings, and this effect was also found to be reduced by BK channel inhibition. These data suggest that (1) disruption of cholesterol-rich microdomains and caveolae by MCD leads to a decrease in the BK channel current thus increasing cell excitability, and (2) the changes in membrane excitability produced by MCD underlie the changes found in Ca(2+) signalling and uterine contractility.
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