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A special issue of Membranes (ISSN 2077-0375). This special issue belongs to the section "Biological Membrane Functions".

Deadline for manuscript submissions: closed (31 March 2022) | Viewed by 45162

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Special Issue Editor

Dr. Tanima Bose

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Leibniz Institute for Neurobiology, Magdeburg, Germany
Interests: ion channels; the role of memory T cells; neuroimmunological diseases; autoimmune ocular surface diseases (OSIDs); immunology and nanoparticle therapy

Special Issue Information

Dear Colleagues,

Physiological processes depend on the continued flow of ions into and out of cells. Ions are more ‘stable’ in water than in the lipid layer inside the membrane. Thus, the hydrophobic membrane acts as a serious energy barrier for transporting ions. In a situation without biological pumps and ion channels, there can be large ion potential differences between the two sides of a biological membrane so that the predominant ions Na+, K+, Ca2+, and Cl- can never cross it. To resolve this issue, ion pumps, ion exchangers (‘active’ transport), and ion channels (‘passive’ transport) are used in cells.

An ion channel needs a single gate and an ion pump works with at least two gates. A gate or a selectivity filter is considered to be a part of a protein that hinders ion movement along the translocation pathway in the prohibitive confirmation but not in the permissive conformation. Ion channels, such as voltage-gated Na+, Ca2+, or K+ channels, are opened when a change of membrane potential displaces the voltage sensors connected to a cytoplasmic side of the ‘activation gate’. They can be closed via reversal of those displacements (‘deactivation’) in response to an opposite change of membrane voltage. However, even with their activation gates in the permissive position, the ion pathway through those channels can be closed through a separate gating process called ‘inactivation’. Both these gates should be in a permissible position for the channel to conduct ions, and closure of either gate obstructs the ion flow. By contrast, ion pumps are controlled via timely cohesion of two gates which are never open simultaneously. Instead, the chosen ions are allowed to enter the pathway from one side of the membrane while one of the gates is open, and then to leave at the other side of the membrane through another gate after the first one shuts down. Although these two transport systems work differently, ion selectivity is a prime criterion for both. The ion pumps generally transport ions against the electrochemical gradient with the use of energy such as adenosine triphosphate (ATP) and a relatively slow speed. By contrast, ion channels are passive transporters of ions with a very high ion conduction rate to maintain the proper membrane potential.

Na+ and K+ are the most abundant cations in biological systems. Na+ ions are most often present at high concentrations outside the cell, and K+ is present at high concentrations inside the cell. Gradients for these ions across the cell membrane provide the energy source for action potentials generated by opening Na+ and K+-channels, and for moving solutes and other ions across the cell membrane via coupled transporters. Among several ions, the gradient for Ca2+ ions is the largest. It helps in controlling several physiological processes such as secretion, excitation, contraction, and cellular proliferation. The cytosol is surrounded by two influxes in the case of immune cells, or negative feedback to terminate the flux by hyperpolarizing the membrane potential and promoting sustained Ca2+-stores: the extracellular space, where the Ca2+ concentration is ~1.8 mM, and massive Ca2+ in the sarco-endoplasmic reticulum (SER), where the Ca2+ concentration varies from 300 μM to 2 mM. In immune cells, intracellular Ca2+ concentration is ~0.1 μM in the resting state, but it is increased 10-fold when the cells are activated.

In conclusion, breakthroughs in the area―especially in membrane potential and ion channels―are especially welcome. Again, this Special Issue offers the perfect site for welcoming the latest innovations, and accordingly, authors from top laboratories are invited to submit their latest results.

Dr. Tanima Bose
Guest Editor

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Keywords

Ion channels
Membrane potential
Calcium signaling
Purinergic signaling
Hyperpolarization and depolarization
Health and disease
Autoimmune and neurodegenerative diseases

Published Papers (14 papers)

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Research

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24 pages, 8222 KiB

Open AccessArticle

Understanding the Dynamics of the Transient and Permanent Opening Events of the Mitochondrial Permeability Transition Pore with a Novel Stochastic Model

by Keertana Yalamanchili, Nasrin Afzal, Liron Boyman, Carmen A. Mannella, W. Jonathan Lederer and M. Saleet Jafri

Membranes 2022, 12(5), 494; https://doi.org/10.3390/membranes12050494 - 30 Apr 2022

Cited by 3 | Viewed by 1663

Abstract

The mitochondrial permeability transition pore (mPTP) is a non-selective pore in the inner mitochondrial membrane (IMM) which causes depolarization when it opens under conditions of oxidative stress and high concentrations of Ca²⁺. In this study, a stochastic computational model was developed to better understand the dynamics of mPTP opening and closing associated with elevated reactive oxygen species (ROS) in cardiomyocytes. The data modeled are from “photon stress” experiments in which the fluorescent dye TMRM (tetramethylrhodamine methyl ester) is both the source of ROS (induced by laser light) and sensor of the electrical potential difference across the IMM. Monte Carlo methods were applied to describe opening and closing of the pore along with the Hill Equation to account for the effect of ROS levels on the transition probabilities. The amplitude distribution of transient mPTP opening events, the number of transient mPTP opening events per minute in a cell, the time it takes for recovery after transient depolarizations in the mitochondria, and the change in TMRM fluorescence during the transition from transient to permanent mPTP opening events were analyzed. The model suggests that mPTP transient open times have an exponential distribution that are reflected in TMRM fluorescence. A second multiple pore model in which individual channels have no permanent open state suggests that 5–10 mPTP per mitochondria would be needed for sustained mitochondrial depolarization at elevated ROS with at least 1 mPTP in the transient open state. Full article

(This article belongs to the Special Issue Membrane Channel of Cells)

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29 pages, 5031 KiB

Open AccessArticle

A Stochastic Spatiotemporal Model of Rat Ventricular Myocyte Calcium Dynamics Demonstrated Necessary Features for Calcium Wave Propagation

by Tuan Minh Hoang-Trong, Aman Ullah, William Jonathan Lederer and Mohsin Saleet Jafri

Membranes 2021, 11(12), 989; https://doi.org/10.3390/membranes11120989 - 18 Dec 2021

Cited by 9 | Viewed by 2420

Abstract

Calcium (Ca²⁺) plays a central role in the excitation and contraction of cardiac myocytes. Experiments have indicated that calcium release is stochastic and regulated locally suggesting the possibility of spatially heterogeneous calcium levels in the cells. This spatial heterogeneity might be important in mediating different signaling pathways. During more than 50 years of computational cell biology, the computational models have been advanced to incorporate more ionic currents, going from deterministic models to stochastic models. While periodic increases in cytoplasmic Ca²⁺ concentration drive cardiac contraction, aberrant Ca²⁺ release can underly cardiac arrhythmia. However, the study of the spatial role of calcium ions has been limited due to the computational expense of using a three-dimensional stochastic computational model. In this paper, we introduce a three-dimensional stochastic computational model for rat ventricular myocytes at the whole-cell level that incorporate detailed calcium dynamics, with (1) non-uniform release site placement, (2) non-uniform membrane ionic currents and membrane buffers, (3) stochastic calcium-leak dynamics and (4) non-junctional or rogue ryanodine receptors. The model simulates spark-induced spark activation and spark-induced Ca²⁺ wave initiation and propagation that occur under conditions of calcium overload at the closed-cell condition, but not when Ca²⁺ levels are normal. This is considered important since the presence of Ca²⁺ waves contribute to the activation of arrhythmogenic currents. Full article

(This article belongs to the Special Issue Membrane Channel of Cells)

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33 pages, 6801 KiB

Open AccessArticle

Cardiac Alternans Occurs through the Synergy of Voltage- and Calcium-Dependent Mechanisms

by Minh Tuan Hoang-Trong, Aman Ullah, William Jonathan Lederer and Mohsin Saleet Jafri

Membranes 2021, 11(10), 794; https://doi.org/10.3390/membranes11100794 - 18 Oct 2021

Cited by 10 | Viewed by 2501

Abstract

Cardiac alternans is characterized by alternating weak and strong beats of the heart. This signaling at the cellular level may appear as alternating long and short action potentials (APs) that occur in synchrony with alternating large and small calcium transients, respectively. Previous studies have suggested that alternans manifests itself through either a voltage dependent mechanism based upon action potential restitution or as a calcium dependent mechanism based on refractoriness of calcium release. We use a novel model of cardiac excitation-contraction (EC) coupling in the rat ventricular myocyte that includes 20,000 calcium release units (CRU) each with 49 ryanodine receptors (RyR2s) and 7 L-type calcium channels that are all stochastically gated. The model suggests that at the cellular level in the case of alternans produced by rapid pacing, the mechanism requires a synergy of voltage- and calcium-dependent mechanisms. The rapid pacing reduces AP duration and magnitude reducing the number of L-type calcium channels activating individual CRUs during each AP and thus increases the population of CRUs that can be recruited stochastically. Elevated myoplasmic and sarcoplasmic reticulum (SR) calcium, [Ca²⁺]_myo and [Ca²⁺]_SR respectively, increases ryanodine receptor open probability (P_o) according to our model used in this simulation and this increased the probability of activating additional CRUs. A CRU that opens in one beat is less likely to open the subsequent beat due to refractoriness caused by incomplete refilling of the junctional sarcoplasmic reticulum (jSR). Furthermore, the model includes estimates of changes in Na⁺ fluxes and [Na⁺]_i and thus provides insight into how changes in electrical activity, [Na⁺]_i and sodium-calcium exchanger activity can modulate alternans. The model thus tracks critical elements that can account for rate-dependent changes in [Na⁺]_i and [Ca²⁺]_myo and how they contribute to the generation of Ca²⁺ signaling alternans in the heart. Full article

(This article belongs to the Special Issue Membrane Channel of Cells)

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17 pages, 1492 KiB

Open AccessArticle

The Changes in Expression of Na_V1.7 and Na_V1.8 and the Effects of the Inhalation of Their Blockers in Healthy and Ovalbumin-Sensitized Guinea Pig Airways

by Michaela Kocmalova, Ivana Kazimierova, Jana Barborikova, Marta Joskova, Sona Franova and Martina Sutovska

Membranes 2021, 11(7), 511; https://doi.org/10.3390/membranes11070511 - 07 Jul 2021

Cited by 3 | Viewed by 2255

Abstract

Background: The presented study evaluated the suppositional changes in the airway expression of Nav1.8 and Nav1.7 and their role in the airway defense mechanisms in healthy animals and in an experimental asthma model. Methods: The effects of the blockers inhalation on the reactivity of guinea pig airways, number of citric-acid-induced coughs and ciliary beating frequency (CBF) were tested in vivo. Chronic inflammation simulating asthma was induced by repetitive exposure to ovalbumin. The expression of Nav1.7 and Nav1.8 was examined by ELISA. Results: The Nav 1.8 blocker showed complex antitussive and bronchodilatory effects and significantly regulated the CBF in healthy and sensitized animals. The Nav1.7 blockers significantly inhibited coughing and participated in CBF control in the ovalbumin-sensitized animals. The increased expression of the respective ion channels in the sensitized animals corresponded to changes in CBF regulation. The therapeutic potency of the Nav1.8 blocker was evidenced in combinations with classic bronchodilators. Conclusion: The allergic-inflammation-upregulated expression of Nav1.7 and Nav1.8 and corresponding effects of blocker inhalation on airway defense mechanisms, along with the Nav1.8 blocker’s compatibility with classic antiasthmatic drugs, bring novel possibilities for the treatment of various respiratory diseases. However, the influence of the Nav1.8 blocker on CBF requires further investigation. Full article

(This article belongs to the Special Issue Membrane Channel of Cells)

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12 pages, 3534 KiB

Open AccessArticle

Extending the Anion Channelrhodopsin-Based Toolbox for Plant Optogenetics

by Yang Zhou, Meiqi Ding, Xiaodong Duan, Kai R. Konrad, Georg Nagel and Shiqiang Gao

Membranes 2021, 11(4), 287; https://doi.org/10.3390/membranes11040287 - 14 Apr 2021

Cited by 9 | Viewed by 2862

Abstract

Optogenetics was developed in the field of neuroscience and is most commonly using light-sensitive rhodopsins to control the neural activities. Lately, we have expanded this technique into plant science by co-expression of a chloroplast-targeted β-carotene dioxygenase and an improved anion channelrhodopsin GtACR1 from the green alga Guillardia theta. The growth of Nicotiana tabacum pollen tube can then be manipulated by localized green light illumination. To extend the application of analogous optogenetic tools in the pollen tube system, we engineered another two ACRs, GtACR2, and ZipACR, which have different action spectra, light sensitivity and kinetic features, and characterized them in Xenopus laevis oocytes, Nicotiana benthamiana leaves and N. tabacum pollen tubes. We found that the similar molecular engineering method used to improve GtACR1 also enhanced GtACR2 and ZipACR performance in Xenopus laevis oocytes. The ZipACR1 performed in N. benthamiana mesophyll cells and N. tabacum pollen tubes with faster kinetics and reduced light sensitivity, allowing for optogenetic control of anion fluxes with better temporal resolution. The reduced light sensitivity would potentially facilitate future application in plants, grown under low ambient white light, combined with an optogenetic manipulation triggered by stronger green light. Full article

(This article belongs to the Special Issue Membrane Channel of Cells)

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11 pages, 5928 KiB

Open AccessArticle

Regulation of K⁺ Conductance by a Hydrogen Bond in Kv2.1, Kv2.2, and Kv1.2 Channels

by Yuchen Zhang, Xuefeng Zhang, Cuiyun Liu and Changlong Hu

Membranes 2021, 11(3), 190; https://doi.org/10.3390/membranes11030190 - 09 Mar 2021

Cited by 5 | Viewed by 1663

Abstract

The slow inactivation of voltage-gated potassium (Kv) channels plays an important role in controlling cellular excitability. Recently, the two hydrogen bonds (H-bonds) formed by W434-D447 and T439-Y445 have been reported to control the slow inactivation in Shaker potassium channels. The four residues are highly conserved among Kv channels. Our objective was to find the roles of the two H-bonds in controlling the slow inactivation of mammalian Kv2.1, Kv2.2, and Kv1.2 channels by point mutation and patch-clamp recording studies. We found that mutations of the residues equivalent to W434 and T439 in Shaker did not change the slow inactivation of the Kv2.1, Kv2.2, and Kv1.2 channels. Surprisingly, breaking of the inter-subunit H-bond formed by W366 and Y376 (Kv2.1 numbering) by various mutations resulted in the complete loss of K⁺ conductance of the three Kv channels. In conclusion, we found differences in the H-bonds controlling the slow inactivation of the mammalian Kv channels and Shaker channels. Our data provided the first evidence, to our knowledge, that the inter-subunit H-bond formed by W366 and Y376 plays an important role in regulating the K⁺ conductance of mammalian Kv2.1, Kv2.2, and Kv1.2 channels. Full article

(This article belongs to the Special Issue Membrane Channel of Cells)

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Review

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19 pages, 1196 KiB

Open AccessReview

Interactions between the Nicotinic and Endocannabinoid Receptors at the Plasma Membrane

by Ana Sofía Vallés and Francisco J. Barrantes

Membranes 2022, 12(8), 812; https://doi.org/10.3390/membranes12080812 - 22 Aug 2022

Cited by 4 | Viewed by 2198

Abstract

Compartmentalization, together with transbilayer and lateral asymmetries, provide the structural foundation for functional specializations at the cell surface, including the active role of the lipid microenvironment in the modulation of membrane-bound proteins. The chemical synapse, the site where neurotransmitter-coded signals are decoded by neurotransmitter receptors, adds another layer of complexity to the plasma membrane architectural intricacy, mainly due to the need to accommodate a sizeable number of molecules in a minute subcellular compartment with dimensions barely reaching the micrometer. In this review, we discuss how nature has developed suitable adjustments to accommodate different types of membrane-bound receptors and scaffolding proteins via membrane microdomains, and how this “effort-sharing” mechanism has evolved to optimize crosstalk, separation, or coupling, where/when appropriate. We focus on a fast ligand-gated neurotransmitter receptor, the nicotinic acetylcholine receptor, and a second-messenger G-protein coupled receptor, the cannabinoid receptor, as a paradigmatic example. Full article

(This article belongs to the Special Issue Membrane Channel of Cells)

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15 pages, 912 KiB

Open AccessReview

Behavior of KCNQ Channels in Neural Plasticity and Motor Disorders

by Som P. Singh, Matthew William, Mira Malavia and Xiang-Ping Chu

Membranes 2022, 12(5), 499; https://doi.org/10.3390/membranes12050499 - 06 May 2022

Viewed by 2575

Abstract

The broad distribution of voltage-gated potassium channels (VGKCs) in the human body makes them a critical component for the study of physiological and pathological function. Within the KCNQ family of VGKCs, these aqueous conduits serve an array of critical roles in homeostasis, especially in neural tissue. Moreover, the greater emphasis on genomic identification in the past century has led to a growth in literature on the role of the ion channels in pathological disease as well. Despite this, there is a need to consolidate the updated findings regarding both the pharmacotherapeutic and pathological roles of KCNQ channels, especially regarding neural plasticity and motor disorders which have the largest body of literature on this channel. Specifically, KCNQ channels serve a remarkable role in modulating the synaptic efficiency required to create appropriate plasticity in the brain. This role can serve as a foundation for clinical approaches to chronic pain. Additionally, KCNQ channels in motor disorders have been utilized as a direction for contemporary pharmacotherapeutic developments due to the muscarinic properties of this channel. The aim of this study is to provide a contemporary review of the behavior of these channels in neural plasticity and motor disorders. Upon review, the behavior of these channels is largely dependent on the physiological role that KCNQ modulatory factors (i.e., pharmacotherapeutic options) serve in pathological diseases. Full article

(This article belongs to the Special Issue Membrane Channel of Cells)

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11 pages, 16121 KiB

Open AccessReview

TRPV4 and PIEZO Channels Mediate the Mechanosensing of Chondrocytes to the Biomechanical Microenvironment

by Min Zhang, Nan Meng, Xiaoxiao Wang, Weiyi Chen and Quanyou Zhang

Membranes 2022, 12(2), 237; https://doi.org/10.3390/membranes12020237 - 18 Feb 2022

Cited by 15 | Viewed by 3512

Abstract

Articular cartilage and their chondrocytes are physiologically submitted to diverse types of mechanical cues. Chondrocytes produce and maintain the cartilage by sensing and responding to changing mechanical loads. TRPV4 and PIEZOs, activated by mechanical cues, are important mechanosensing molecules of chondrocytes and have pivotal roles in articular cartilage during health and disease. The objective of this review is to introduce the recent progress indicating that the mechanosensitive ion channels, TRPV4 and PIEZOs, are involved in the chondrocyte sensing of mechanical and inflammatory cues. We present a focus on the important role of TRPV4 and PIEZOs in the mechanotransduction regulating diverse chondrocyte functions in the biomechanical microenvironment. The review synthesizes the most recent advances in our understanding of how mechanical stimuli affect various cellular behaviors and functions through differentially activating TRPV4 and PIEZO ion channels in chondrocyte. Advances in understanding the complex roles of TRPV4/PIEZO-mediated mechanosignaling mechanisms have the potential to recapitulate physiological biomechanical microenvironments and design cell-instructive biomaterials for cartilage tissue engineering. Full article

(This article belongs to the Special Issue Membrane Channel of Cells)

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19 pages, 3299 KiB

Open AccessReview

P-Loop Channels: Experimental Structures, and Physics-Based and Neural Networks-Based Models

by Denis B. Tikhonov and Boris S. Zhorov

Membranes 2022, 12(2), 229; https://doi.org/10.3390/membranes12020229 - 16 Feb 2022

Cited by 6 | Viewed by 2886

Abstract

The superfamily of P-loop channels includes potassium, sodium, and calcium channels, as well as TRP channels and ionotropic glutamate receptors. A rapidly increasing number of crystal and cryo-EM structures have revealed conserved and variable elements of the channel structures. Intriguing differences are seen in transmembrane helices of channels, which may include π-helical bulges. The bulges reorient residues in the helices and thus strongly affect their intersegment contacts and patterns of ligand-sensing residues. Comparison of the experimental structures suggests that some π-bulges are dynamic: they may appear and disappear upon channel gating and ligand binding. The AlphaFold2 models represent a recent breakthrough in the computational prediction of protein structures. We compared some crystal and cryo-EM structures of P-loop channels with respective AlphaFold2 models. Folding of the regions, which are resolved experimentally, is generally similar to that predicted in the AlphaFold2 models. The models also reproduce some subtle but significant differences between various P-loop channels. However, patterns of π-bulges do not necessarily coincide in the experimental and AlphaFold2 structures. Given the importance of dynamic π-bulges, further studies involving experimental and theoretical approaches are necessary to understand the cause of the discrepancy. Full article

(This article belongs to the Special Issue Membrane Channel of Cells)

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14 pages, 364 KiB

Open AccessReview

Acid-Sensing Ion Channels in Glial Cells

by Victoria Cegielski, Rohan Chakrabarty, Shinghua Ding, Michael J. Wacker, Paula Monaghan-Nichols and Xiang-Ping Chu

Membranes 2022, 12(2), 119; https://doi.org/10.3390/membranes12020119 - 20 Jan 2022

Cited by 8 | Viewed by 3113

Abstract

Acid-sensing ion channels (ASICs) are proton-gated cation channels and key mediators of responses to neuronal injury. ASICs exhibit unique patterns of distribution in the brain, with high expression in neurons and low expression in glial cells. While there has been a lot of focus on ASIC in neurons, less is known about the roles of ASICs in glial cells. ASIC1a is expressed in astrocytes and might contribute to synaptic transmission and long-term potentiation. In oligodendrocytes, constitutive activation of ASIC1a participates in demyelinating diseases. ASIC1a, ASIC2a, and ASIC3, found in microglial cells, could mediate the inflammatory response. Under pathological conditions, ASIC dysregulation in glial cells can contribute to disease states. For example, activation of astrocytic ASIC1a may worsen neurodegeneration and glioma staging, activation of microglial ASIC1a and ASIC2a may perpetuate ischemia and inflammation, while oligodendrocytic ASIC1a might be involved in multiple sclerosis. This review concentrates on the unique ASIC components in each of the glial cells and integrates these glial-specific ASICs with their physiological and pathological conditions. Such knowledge provides promising evidence for targeting of ASICs in individual glial cells as a therapeutic strategy for a diverse range of conditions. Full article

(This article belongs to the Special Issue Membrane Channel of Cells)

21 pages, 9376 KiB

Open AccessReview

Acid-Sensing Ion Channel 2: Function and Modulation

by Andy Sivils, Felix Yang, John Q. Wang and Xiang-Ping Chu

Membranes 2022, 12(2), 113; https://doi.org/10.3390/membranes12020113 - 19 Jan 2022

Cited by 8 | Viewed by 4652

Abstract

Acid-sensing ion channels (ASICs) have an important influence on human physiology and pathology. They are members of the degenerin/epithelial sodium channel family. Four genes encode at least six subunits, which combine to form a variety of homotrimers and heterotrimers. Of these, ASIC1a homotrimers and ASIC1a/2 heterotrimers are most widely expressed in the central nervous system (CNS). Investigations into the function of ASIC1a in the CNS have revealed a wealth of information, culminating in multiple contemporary reviews. The lesser-studied ASIC2 subunits are in need of examination. This review will focus on ASIC2 in health and disease, with discussions of its role in modulating ASIC function, synaptic targeting, cardiovascular responses, and pharmacology, while exploring evidence of its influence in pathologies such as ischemic brain injury, multiple sclerosis, epilepsy, migraines, drug addiction, etc. This information substantiates the ASIC2 protein as a potential therapeutic target for various neurological, psychological, and cerebrovascular diseases. Full article

(This article belongs to the Special Issue Membrane Channel of Cells)

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19 pages, 2406 KiB

Open AccessReview

Homomeric and Heteromeric α7 Nicotinic Acetylcholine Receptors in Health and Some Central Nervous System Diseases

by Virginia Borroni and Francisco J. Barrantes

Membranes 2021, 11(9), 664; https://doi.org/10.3390/membranes11090664 - 29 Aug 2021

Cited by 21 | Viewed by 4320

Abstract

Nicotinic acetylcholine receptors (nAChRs) are pentameric ligand-gated ion channels involved in the modulation of essential brain functions such as memory, learning, and attention. Homomeric α7 nAChR, formed exclusively by five identical α7 subunits, is involved in rapid synaptic transmission, whereas the heteromeric oligomers composed of α7 in combination with β subunits display metabotropic properties and operate in slower time frames. At the cellular level, the activation of nAChRs allows the entry of Na⁺ and Ca²⁺; the two cations depolarize the membrane and trigger diverse cellular signals, depending on the type of nAChR pentamer and neurons involved, the location of the intervening cells, and the networks of which these neuronal cells form part. These features make the α7 nAChR a central player in neurotransmission, metabolically associated Ca²⁺-mediated signaling, and modulation of diverse fundamental processes operated by other neurotransmitters in the brain. Due to its ubiquitous distribution and the multiple functions it displays in the brain, the α7 nAChR is associated with a variety of neurological and neuropsychiatric disorders whose exact etiopathogenic mechanisms are still elusive. Full article

(This article belongs to the Special Issue Membrane Channel of Cells)

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15 pages, 1885 KiB

Open AccessReview

Polyunsaturated Fatty Acids Mediated Regulation of Membrane Biochemistry and Tumor Cell Membrane Integrity

by Souvik Mukerjee, Abdulaziz S. Saeedan, Mohd. Nazam Ansari and Manjari Singh

Membranes 2021, 11(7), 479; https://doi.org/10.3390/membranes11070479 - 28 Jun 2021

Cited by 22 | Viewed by 6896

Abstract

Particular dramatic macromolecule proteins are responsible for various cellular events in our body system. Lipids have recently recognized a lot more attention of scientists for understanding the relationship between lipid and cellular function and human health However, a biological membrane is formed with a lipid bilayer, which is called a P–L–P design. Our body system is balanced through various communicative signaling pathways derived from biological membrane proteins and lipids. In the case of any fatal disease such as cancer, the biological membrane compositions are altered. To repair the biological membrane composition and prevent cancer, dietary fatty acids, such as omega-3 polyunsaturated fatty acids, are essential in human health but are not directly synthesized in our body system. In this review, we will discuss the alteration of the biological membrane composition in breast cancer. We will highlight the role of dietary fatty acids in altering cellular composition in the P–L–P bilayer. We will also address the importance of omega-3 polyunsaturated fatty acids to regulate the membrane fluidity of cancer cells. Full article

(This article belongs to the Special Issue Membrane Channel of Cells)

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