scholarly journals Non-genomic effects of steroid hormones: role of ion channels

2019 ◽  
pp. 3-12 ◽  
Author(s):  
Darya Y. Straltsova ◽  
Maryia A. Charnysh ◽  
Palina V. Hryvusevich ◽  
Vadim V. Demidchik
Keyword(s):  
Ion Channels ◽  
Ion Channel ◽  
Steroid Hormones ◽  
Plant Cells ◽  
Membrane Receptors ◽  
Physiological Effects ◽  
Genomic Effects

In animals, steroid hormones can act using genomic and non-genomic mechanisms. Plant steroid hormones, brassinosteroids, are capable of inducing the expression of some gene ensembles, however their non-genomic pathways for triggering the physiological effects are still unclear. In this paper, we propose the hypothesis on existence of brassinosteroid non-genomic effects in plant cells. This non-genomic pathway could due to modulation of ion channel activities and modification of membrane receptors.

Progesterone interaction with sperm plasma membrane, calcium influx and induction of the acrosome reaction

1999 ◽  
Vol 7 (2) ◽  
pp. 81-93 ◽  
Author(s):  
Christopher Bray ◽  
Jackson CK Brown ◽  
Steve Publicover ◽  
Christopher LR Barratt
Keyword(s):  
Plasma Membrane ◽  
Steroid Hormones ◽  
Nuclear Receptors ◽  
Acrosome Reaction ◽  
Calcium Influx ◽  
Membrane Receptors ◽  
Sperm Plasma Membrane ◽  
The Subject ◽  
Genomic Effects ◽  
Intense Research

In contrast to the classic action of steroid hormones through cytoplasmic/nuclear receptors, there is an accumulating body of data which strongly suggests that they have a direct effect on cells mediated through putative membrane receptors, a so-called non-genomic action. Although such non-genomic effects were discovered 50 years ago it is only in the last 15 years that the subject has become an area of intense research.

scholarly journals Phosphorylation-Dependent Regulation of Ryanodine Receptors

2001 ◽  
Vol 153 (4) ◽  
pp. 699-708 ◽  
Author(s):  
Steven O. Marx ◽  
Steven Reiken ◽  
Yuji Hisamatsu ◽  
Marta Gaburjakova ◽  
Jana Gaburjakova ◽  
...  
Keyword(s):  
Ion Channels ◽  
Ion Channel ◽  
Calcium Release ◽  
Ryanodine Receptors ◽  
Rapid Identification ◽  
Calcium Release Channels ◽  
Macromolecular Complexes ◽  
Protein Binding Sites ◽  
Skeletal Muscle Contraction

Ryanodine receptors (RyRs), intracellular calcium release channels required for cardiac and skeletal muscle contraction, are macromolecular complexes that include kinases and phosphatases. Phosphorylation/dephosphorylation plays a key role in regulating the function of many ion channels, including RyRs. However, the mechanism by which kinases and phosphatases are targeted to ion channels is not well understood. We have identified a novel mechanism involved in the formation of ion channel macromolecular complexes: kinase and phosphatase targeting proteins binding to ion channels via leucine/isoleucine zipper (LZ) motifs. Activation of kinases and phosphatases bound to RyR2 via LZs regulates phosphorylation of the channel, and disruption of kinase binding via LZ motifs prevents phosphorylation of RyR2. Elucidation of this new role for LZs in ion channel macromolecular complexes now permits: (a) rapid mapping of kinase and phosphatase targeting protein binding sites on ion channels; (b) predicting which kinases and phosphatases are likely to regulate a given ion channel; (c) rapid identification of novel kinase and phosphatase targeting proteins; and (d) tools for dissecting the role of kinases and phosphatases as modulators of ion channel function.

Actin dynamics as critical ion channel regulator: ENaC and Piezo in focus

2021 ◽  
Author(s):  
Elena A. Morachevskaya ◽  
Anastasia V. Sudarikova
Keyword(s):  
Ion Channels ◽  
Ion Channel ◽  
Dynamic Balance ◽  
Cell Volume Regulation ◽  
Actin Dynamics ◽  
Actin Binding ◽  
Actin Assembly ◽  
Excitable Cells ◽  
Physiological Processes

Ion channels in plasma membrane play a principal role in different physiological processes, including cell volume regulation, signal transduction and modulation of membrane potential in living cells. Actin-based cytoskeleton, which exists in a dynamic balance between monomeric and polymeric forms (globular and fibrillar actin), can be directly or indirectly involved in various cellular responses including modulation of ion channel activity. In this mini-review, we present an overview of the role of submembranous actin dynamics in the regulation of ion channels in excitable and non-excitable cells. Special attention is focused on the important data about the involvement of actin assembly/disassembly and some actin-binding proteins in the control of the Epithelial Na+ Channel (ENaC) and mechanosensitive Piezo channels whose integral activity has potential impact on membrane transport and multiple coupled cellular reactions. Growing evidence suggests that actin elements of the cytoskeleton can represent a "converging point" of various signaling pathways modulating the activity of ion transport proteins in cell membranes.

scholarly journals Human sperm ion channel (dys)function: implications for fertilization

2019 ◽  
Vol 25 (6) ◽  
pp. 758-776 ◽  
Author(s):  
Sean G Brown ◽  
Stephen J Publicover ◽  
Christopher L R Barratt ◽  
Sarah J Martins da Silva
Keyword(s):  
Ion Channels ◽  
Ion Channel ◽  
Potassium Currents ◽  
Human Sperm ◽  
Clinical Samples ◽  
Knock Out ◽  
Infertile Men ◽  
Human Fertility ◽  
Potassium Conductances

Abstract BACKGROUND Intensive research on sperm ion channels has identified members of several ion channel families in both mouse and human sperm. Gene knock-out studies have unequivocally demonstrated the importance of the calcium and potassium conductances in sperm for fertility. In both species, the calcium current is carried by the highly complex cation channel of sperm (CatSper). In mouse sperm, the potassium current has been conclusively shown to be carried by a channel consisting of the pore forming subunit SLO3 and auxiliary subunit leucine-rich repeat-containing 52 (LRRC52). However, in human sperm it is controversial whether the pore forming subunit of the channel is composed of SLO3 and/or SLO1. Deciphering the role of the proton-specific Hv1 channel is more challenging as it is only expressed in human sperm. However, definitive evidence for a role in, and importance for, human fertility can only be determined through studies using clinical samples. OBJECTIVE AND RATIONALE This review aims to provide insight into the role of sperm ion channels in human fertilization as evidenced from recent studies of sperm from infertile men. We also summarize the key discoveries from mouse ion channel knock-out models and contrast the properties of mouse and human CatSper and potassium currents. We detail the evidence for, and consequences of, defective ion channels in human sperm and discuss hypotheses to explain how defects arise and why affected sperm have impaired fertilization potential. SEARCH METHODS Relevant studies were identified using PubMed and were limited to ion channels that have been characterized in mouse and human sperm. Additional notable examples from other species are included as appropriate. OUTCOMES There are now well-documented fundamental differences between the properties of CatSper and potassium channel currents in mouse and human sperm. However, in both species, sperm lacking either channel cannot fertilize in vivo and CatSper-null sperm also fail to fertilize at IVF. Sperm-lacking potassium currents are capable of fertilizing at IVF, albeit at a much lower rate. However, additional complex and heterogeneous ion channel dysfunction has been reported in sperm from infertile men, the causes of which are unknown. Similarly, the nature of the functional impairment of affected patient sperm remains elusive. There are no reports of studies of Hv1 in human sperm from infertile men. WIDER IMPLICATIONS Recent studies using sperm from infertile men have given new insight and critical evidence supporting the supposition that calcium and potassium conductances are essential for human fertility. However, it should be highlighted that many fundamental questions remain regarding the nature of molecular and functional defects in sperm with dysfunctional ion channels. The development and application of advanced technologies remains a necessity to progress basic and clinical research in this area, with the aim of providing effective screening methodologies to identify and develop treatments for affected men in order to help prevent failed ART cycles. Conversely, development of drugs that block calcium and/or potassium conductances in sperm is a plausible strategy for producing sperm-specific contraceptives.

scholarly journals Role of Sex Steroid Hormones in Bacterial-Host Interactions

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Elizabeth García-Gómez ◽  
Bertha González-Pedrajo ◽  
Ignacio Camacho-Arroyo
Keyword(s):  
Steroid Hormones ◽  
Bacterial Infections ◽  
Pathogenic Bacteria ◽  
Sex Steroid Hormones ◽  
Membrane Receptors ◽  
Sex Steroid ◽  
Bacterial Host ◽  
Host Interactions ◽  
Environmental Bacteria

Sex steroid hormones play important physiological roles in reproductive and nonreproductive tissues, including immune cells. These hormones exert their functions by binding to either specific intracellular receptors that act as ligand-dependent transcription factors or membrane receptors that stimulate several signal transduction pathways. The elevated susceptibility of males to bacterial infections can be related to the usually lower immune responses presented in males as compared to females. This dimorphic sex difference is mainly due to the differential modulation of the immune system by sex steroid hormones through the control of proinflammatory and anti-inflammatory cytokines expression, as well as Toll-like receptors (TLRs) expression and antibody production. Besides, sex hormones can also affect the metabolism, growth, or virulence of pathogenic bacteria. In turn, pathogenic, microbiota, and environmental bacteria are able to metabolize and degrade steroid hormones and their related compounds. All these data suggest that sex steroid hormones play a key role in the modulation of bacterial-host interactions.

scholarly journals Computational biology in the study of cardiac ion channels and cell electrophysiology

2006 ◽  
Vol 39 (1) ◽  
pp. 57-116 ◽  
Author(s):  
Yoram Rudy ◽  
Jonathan R. Silva
Keyword(s):  
Ion Channels ◽  
Action Potential ◽  
Ion Channel ◽  
Markov Models ◽  
Cardiac Action Potential ◽  
Genetic Mutations ◽  
Cardiac Ion Channels ◽  
Cardiac Action ◽  
Ion Channel Kinetics

1. Prologue 582. The Hodgkin–Huxley formalism for computing the action potential 592.1 The axon action potential model 592.2 Cardiac action potential models 623. Ion-channel based formulation of the action potential 653.1 Ion-channel structure 653.2 Markov models of ion-channel kinetics 663.3 Role of selected ion channels in rate dependence of the cardiac action potential 713.4 Physiological implications of IKs subunit interaction 773.5 Mechanism of cardiac action potential rate-adaptation is species dependent 784. Simulating ion-channel mutations and their electrophysiological consequences 814.1 Mutations in SCN5A, the gene that encodes the cardiac sodium channel 824.1.1 The ΔKPQ mutation and LQT3 824.1.2 SCN5A mutation that underlies a dual phenotype 874.2 Mutations in HERG, the gene that encodes IKr: re-examination of the ‘gain of function/loss of function’ concept 944.3 Role of IKs as ‘repolarization reserve’ 1005. Modeling cell signaling in electrophysiology 1025.1 CaMKII regulation of the Ca2+ transient 1025.2 The β-adrenergic signaling cascade 1056. Epilogue 1077. Acknowledgments 1088. References 109The cardiac cell is a complex biological system where various processes interact to generate electrical excitation (the action potential, AP) and contraction. During AP generation, membrane ion channels interact nonlinearly with dynamically changing ionic concentrations and varying transmembrane voltage, and are subject to regulatory processes. In recent years, a large body of knowledge has accumulated on the molecular structure of cardiac ion channels, their function, and their modification by genetic mutations that are associated with cardiac arrhythmias and sudden death. However, ion channels are typically studied in isolation (in expression systems or isolated membrane patches), away from the physiological environment of the cell where they interact to generate the AP. A major challenge remains the integration of ion-channel properties into the functioning, complex and highly interactive cell system, with the objective to relate molecular-level processes and their modification by disease to whole-cell function and clinical phenotype. In this article we describe how computational biology can be used to achieve such integration. We explain how mathematical (Markov) models of ion-channel kinetics are incorporated into integrated models of cardiac cells to compute the AP. We provide examples of mathematical (computer) simulations of physiological and pathological phenomena, including AP adaptation to changes in heart rate, genetic mutations in SCN5A and HERG genes that are associated with fatal cardiac arrhythmias, and effects of the CaMKII regulatory pathway and β-adrenergic cascade on the cell electrophysiological function.

scholarly journals Ion Channel Dysfunction and Neuroinflammation in Migraine and Depression

2021 ◽  
Vol 12 ◽  
Author(s):  
Emine Eren-Koçak ◽  
Turgay Dalkara
Keyword(s):  
Ion Channels ◽  
Ion Channel ◽  
Energy Homeostasis ◽  
Inflammatory Signaling ◽  
Pannexin 1 ◽  
Significant Heritability ◽  
Homeostatic Function ◽  
And Function ◽  
Excitability Of Neurons

Migraine and major depression are debilitating disorders with high lifetime prevalence rates. Interestingly these disorders are highly comorbid and show significant heritability, suggesting shared pathophysiological mechanisms. Non-homeostatic function of ion channels and neuroinflammation may be common mechanisms underlying both disorders: The excitation-inhibition balance of microcircuits and their modulation by monoaminergic systems, which depend on the expression and function of membrane located K+, Na+, and Ca+2 channels, have been reported to be disturbed in both depression and migraine. Ion channels and energy supply to synapses not only change excitability of neurons but can also mediate the induction and maintenance of inflammatory signaling implicated in the pathophysiology of both disorders. In this respect, Pannexin-1 and P2X7 large-pore ion channel receptors can induce inflammasome formation that triggers release of pro-inflammatory mediators from the cell. Here, the role of ion channels involved in the regulation of excitation-inhibition balance, synaptic energy homeostasis as well as inflammatory signaling in migraine and depression will be reviewed.

scholarly journals Mining recent brain proteomic databases for ion channel phosphosite nuggets

2010 ◽  
Vol 137 (1) ◽  
pp. 3-16 ◽  
Author(s):  
Oscar Cerda ◽  
Je-Hyun Baek ◽  
James S. Trimmer
Keyword(s):  
Ion Channels ◽  
Ion Channel ◽  
Mammalian Brain ◽  
Phosphorylation Sites ◽  
Dynamic Regulation ◽  
Voltage Gated ◽  
Voltage Gated Ion Channels ◽  
Α Subunits

Voltage-gated ion channels underlie electrical activity of neurons and are dynamically regulated by diverse cell signaling pathways that alter their phosphorylation state. Recent global mass spectrometric–based analyses of the mouse brain phosphoproteome have yielded a treasure trove of new data as to the extent and nature of phosphorylation of numerous ion channel principal or α subunits in mammalian brain. Here we compile and review data on 347 phosphorylation sites (261 unique) on 42 different voltage-gated ion channel α subunits that were identified in these recent studies. Researchers in the ion channel field can now begin to explore the role of these novel in vivo phosphorylation sites in the dynamic regulation of the localization, activity, and expression of brain ion channels through multisite phosphorylation of their principal subunits.

scholarly journals Speed, adaptation, and stability of the response to light in cone photoreceptors: The functional role of Ca-dependent modulation of ligand sensitivity in cGMP-gated ion channels

2011 ◽  
Vol 139 (1) ◽  
pp. 31-56 ◽  
Author(s):  
Juan I. Korenbrot
Keyword(s):  
Ion Channels ◽  
Ion Channel ◽  
Critical Role ◽  
Enzymatic Reactions ◽  
Cone Photoreceptors ◽  
Channel Modulation ◽  
Ion Channel Modulation ◽  
Gated Ion Channels ◽  
Ligand Sensitivity

The response of cone photoreceptors to light is stable and reproducible because of the exceptional regulation of the cascade of enzymatic reactions that link visual pigment (VP) excitation to the gating of cyclic GMP (cGMP)-gated ion channels (cyclic nucleotide–gated [CNG]) in the outer segment plasma membrane. Regulation is achieved in part through negative feedback control of some of these reactions by cytoplasmic free Ca2+. As part of the control process, Ca2+ regulates the phosphorylation of excited VP, the activity of guanylate cyclase, and the ligand sensitivity of the CNG ion channels. We measured photocurrents elicited by stimuli in the form of flashes, steps, and flashes superimposed on steps in voltage-clamped single bass cones isolated from striped bass retina. We also developed a computational model that comprises all the known molecular events of cone phototransduction, including all Ca-dependent controls. Constrained by available experimental data in bass cones and cone transduction biochemistry, we achieved an excellent match between experimental photocurrents and those simulated by the model. We used the model to explore the physiological role of CNG ion channel modulation. Control of CNG channel activity by both cGMP and Ca2+ causes the time course of the light-dependent currents to be faster than if only cGMP controlled their activity. Channel modulation also plays a critical role in the regulation of the light sensitivity and light adaptation of the cone photoresponse. In the absence of ion channel modulation, cone photocurrents would be unstable, oscillating during and at the offset of light stimuli.

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