scholarly journals Functional clustering and coupling of ion channels in cellular mechanosensing is independent on lipid raft integrity in plasma membrane

2020 ◽  
Vol 1867 (10) ◽  
pp. 118764
Author(s):  
Vladislav I. Chubinskiy-Nadezhdin ◽  
Valeria Y. Vasileva ◽  
Yuri A. Negulyaev ◽  
Elena A. Morachevskaya
Keyword(s):  
Plasma Membrane ◽  
Ion Channels ◽  
Lipid Raft ◽  
Functional Clustering ◽  
Cellular Mechanosensing

scholarly journals Cannabinoid receptors distribution in mouse cortical plasma membrane compartments

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Hajar Miranzadeh Mahabadi ◽  
Haseeb Bhatti ◽  
Robert B. Laprairie ◽  
Changiz Taghibiglou
Keyword(s):  
Plasma Membrane ◽  
Lipid Raft ◽  
Cannabinoid Receptors ◽  
Gradient Centrifugation ◽  
Brain Regions ◽  
Cb1 Receptor ◽  
The Body ◽  
Cb2 Receptor ◽  
Cortical Tissue ◽  
Ionic Detergent

AbstractThe type 1 and type 2 cannabinoid receptors (CB1 and CB2 receptors) are class A G protein-coupled receptors (GPCRs) that are activated by endogenous lipids called endocannabinoids to modulate neuronal excitability and synaptic transmission in neurons throughout the central nervous system (CNS), and inflammatory processes throughout the body. CB1 receptor is one of the most abundant GPCRs in the CNS and is involved in many physiological and pathophysiological processes, including mood, appetite, and nociception. CB2 receptor is primarily found on immunomodulatory cells of both the CNS and the peripheral immune system. In this study, we isolated lipid raft and non-lipid raft fractions of plasma membrane (PM) from mouse cortical tissue by using cold non-ionic detergent and sucrose gradient centrifugation to study the localization of CB1 receptor and CB2 receptor. Lipid raft and non-lipid raft fractions were confirmed by flotillin-1, caveolin-1 and transferrin receptor as their protein biomarkers. Both CB1 receptor and CB2 receptor were found in non-raft compartments that is inconsistent with previous findings in cultured cell lines. This study demonstrates compartmentalization of both CB1 receptor and CB2 receptor in cortical tissue and warrants further investigation of CB1 receptor and CB2 receptor compartmental distribution in various brain regions and cell types.

scholarly journals RalA and RalB Proteins Are Ubiquitinated GTPases, and Ubiquitinated RalA Increases Lipid Raft Exposure at the Plasma Membrane

2012 ◽  
Vol 287 (35) ◽  
pp. 29397-29405 ◽  
Author(s):  
Vincent Neyraud ◽  
Vasily N. Aushev ◽  
Anastassia Hatzoglou ◽  
Brigitte Meunier ◽  
Ilaria Cascone ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Lipid Raft

scholarly journals Lipid raft–dependent plasma membrane repair interferes with the activation of B lymphocytes

2015 ◽  
Vol 211 (6) ◽  
pp. 1193-1205 ◽  
Author(s):  
Heather Miller ◽  
Thiago Castro-Gomes ◽  
Matthias Corrotte ◽  
Christina Tam ◽  
Timothy K. Maugel ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
B Cell ◽  
B Lymphocytes ◽  
Lipid Rafts ◽  
Lipid Raft ◽  
Cell Activation ◽  
Dependent Manner ◽  
B Cell Activation ◽  
Membrane Repair ◽  
Membrane Injury

Cells rapidly repair plasma membrane (PM) damage by a process requiring Ca2+-dependent lysosome exocytosis. Acid sphingomyelinase (ASM) released from lysosomes induces endocytosis of injured membrane through caveolae, membrane invaginations from lipid rafts. How B lymphocytes, lacking any known form of caveolin, repair membrane injury is unknown. Here we show that B lymphocytes repair PM wounds in a Ca2+-dependent manner. Wounding induces lysosome exocytosis and endocytosis of dextran and the raft-binding cholera toxin subunit B (CTB). Resealing is reduced by ASM inhibitors and ASM deficiency and enhanced or restored by extracellular exposure to sphingomyelinase. B cell activation via B cell receptors (BCRs), a process requiring lipid rafts, interferes with PM repair. Conversely, wounding inhibits BCR signaling and internalization by disrupting BCR–lipid raft coclustering and by inducing the endocytosis of raft-bound CTB separately from BCR into tubular invaginations. Thus, PM repair and B cell activation interfere with one another because of competition for lipid rafts, revealing how frequent membrane injury and repair can impair B lymphocyte–mediated immune responses.

Pharmacology and Regulation of the Ion Channels of the Brown Adipocyte Plasma Membrane

1994 ◽  
pp. 103-108
Author(s):  
A. Koivisto ◽  
T. Ringer ◽  
U. Ruß ◽  
J. Nedergaard ◽  
D. Siemen
Keyword(s):  
Plasma Membrane ◽  
Ion Channels ◽  
Brown Adipocyte

scholarly journals Analgesic Effects of Lipid Raft Disruption by Sphingomyelinase and Myriocin via Transient Receptor Potential Vanilloid 1 and Transient Receptor Potential Ankyrin 1 Ion Channel Modulation

2021 ◽  
Vol 11 ◽  
Author(s):  
Ádám Horváth ◽  
Maja Payrits ◽  
Anita Steib ◽  
Boglárka Kántás ◽  
Tünde Biró-Süt ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Lipid Raft ◽  
Transient Receptor Potential ◽  
Trp Channels ◽  
Receptor Potential ◽  
Membrane Microdomains ◽  
Neuronal Cultures ◽  
Transient Receptor Potential Vanilloid ◽  
Peripheral Sensitization ◽  
Transient Receptor

Transient Receptor Potential (TRP) Vanilloid 1 and Ankyrin 1 (TRPV1, TRPA1) cation channels are expressed in nociceptive primary sensory neurons, and integratively regulate nociceptor and inflammatory functions. Lipid rafts are liquid-ordered plasma membrane microdomains rich in cholesterol, sphingomyelin and gangliosides. We earlier showed that lipid raft disruption inhibits TRPV1 and TRPA1 functions in primary sensory neuronal cultures. Here we investigated the effects of sphingomyelinase (SMase) cleaving membrane sphingomyelin and myriocin (Myr) prohibiting sphingolipid synthesis in mouse pain models of different mechanisms. SMase (50 mU) or Myr (1 mM) pretreatment significantly decreased TRPV1 activation (capsaicin)-induced nocifensive eye-wiping movements by 37 and 41%, respectively. Intraplantar pretreatment by both compounds significantly diminished TRPV1 stimulation (resiniferatoxin)-evoked thermal allodynia developing mainly by peripheral sensitization. SMase (50 mU) also decreased mechanical hyperalgesia related to both peripheral and central sensitizations. SMase (50 mU) significantly reduced TRPA1 activation (formalin)-induced acute nocifensive behaviors by 64% in the second, neurogenic inflammatory phase. Myr, but not SMase altered the plasma membrane polarity related to the cholesterol composition as shown by fluorescence spectroscopy. These are the first in vivo results showing that sphingolipids play a key role in lipid raft integrity around nociceptive TRP channels, their activation and pain sensation. It is concluded that local SMase administration might open novel perspective for analgesic therapy.

scholarly journals Carboxamido steroids inhibit the opening properties of transient receptor potential ion channels by lipid raft modulation

2018 ◽  
Vol 59 (10) ◽  
pp. 1851-1863 ◽  
Author(s):  
Éva Sághy ◽  
Maja Payrits ◽  
Tünde Bíró-Sütő ◽  
Rita Skoda-Földes ◽  
Eszter Szánti-Pintér ◽  
...  
Keyword(s):  
Ion Channels ◽  
Lipid Raft ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor

Abstract 44: Reactive Oxygen Species Mediate TLR4 MyD88 Independent Signaling in Human Hemoglobin-Associated Macrophages Through TLR4 Lipid Raft Interactions

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Aloke Finn ◽  
Masataka Nakano ◽  
Rohini Polavarapu ◽  
Vinit Karmali ◽  
Omar Saeed ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Plasma Membrane ◽  
Lipid Raft ◽  
Foam Cell ◽  
Large Fraction ◽  
Reactive Oxygen ◽  
Intraplaque Hemorrhage ◽  
Oxygen Species ◽  
Intracellular Iron ◽  
Lps Treatment

Objectives: Experimental data indicate an important role for Toll-like Receptor 4 (TLR4) MyD88 independent signaling in upregulating Interferon β (IFN-β) production and driving atherosclerosis. We recently identified a distinct non-foam cell macrophage (M(Hb) or Hb-associated macrophage) in areas of intraplaque hemorrhage characterized by reduced reactive oxygen species (ROS) and pro-inflammatory cytokines. In this study, we investigated the role of iron and ROS in mediating TLR4 MyD88 independent signaling in these cells. Methods and Results: Areas rich in M(Hb) in atherosclerotic plaques demonstrated significantly reduced IFN-β expression compared to foam cell areas by immunostaining and quantitative PCR. M(Hb) did not upregulate IFN-β when exposed to ox LDL in contrast to control macrophages, a response which was inhibited in the presence of a TLR4 blocking antibody. To further investigate TLR4 responses in M(Hb), we used the TLR4 activator LPS. LPS produced significant increases in IFN-β in control macrophages but had no effect in M(Hb). This defect could be corrected by raising intracellular iron by pretreating M(Hb) with hepcidin prior to LPS treatment, suggesting redox state mediates this effect. The interaction of TLR4 with TRIF was examined by immunoprecipitation of lysates from control or M(Hb) cells treated with LPS using a TLR4 antibody and immunoblotting for TRIF. LPS treatment of control but not M(Hb) cells resulted in an increase in TRIF. Hepcidin pretreatment of M(Hb) corrected this interaction in response to LPS while differentiating monocytes in superoxide dismutase prevented it. Lastly, the interaction between lipid rafts and TLR4 was examined using FITC-cholera toxin (CTx) and a TLR4 antibody. In control cells the distribution of CTx on the plasma membrane was homogeneous and TLR4 localized to both the membrane and intracellular compartment. After LPS, a large fraction of TLR4 translocated to the plasma membrane, and colocalization of TLR4 and CTx was observed. In M(Hb) the LPS- induced translocation of TLR4 to the membrane rafts was inhibited. Conclusion: M(Hb) cells modulate TLR4 MyD88 independent signaling through reducing ROS which inhibits TLR4 lipid raft interactions.

Ion Channels in the Plasma Membrane of Plant Cells

1992 ◽  
pp. 225-236
Author(s):  
B. R. Terry ◽  
S. D. Tyerman ◽  
G. P. Findlay
Keyword(s):  
Plasma Membrane ◽  
Ion Channels ◽  
Plant Cells

scholarly journals Moderate Static Magnetic Field (6 mT)-Induced Lipid Rafts Rearrangement Increases Silver NPs Uptake in Human Lymphocytes

Molecules ◽  
2020 ◽  
Vol 25 (6) ◽  
pp. 1398
Author(s):  
Cristian Vergallo ◽  
Elisa Panzarini ◽  
Bernardetta Anna Tenuzzo ◽  
Stefania Mariano ◽  
Ada Maria Tata ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Lipid Rafts ◽  
Lipid Raft ◽  
Human Lymphocytes ◽  
Peripheral Blood Lymphocytes ◽  
Membrane Lipid ◽  
Membrane Perturbation ◽  
Plasma Membrane Lipid ◽  
Silver Nps ◽  
Surface Ligand

One of the most relevant drawbacks in medicine is the ability of drugs and/or imaging agents to reach cells. Nanotechnology opened new horizons in drug delivery, and silver nanoparticles (AgNPs) represent a promising delivery vehicle for their adjustable size and shape, high-density surface ligand attachment, etc. AgNPs cellular uptake involves different endocytosis mechanisms, including lipid raft-mediated endocytosis. Since static magnetic fields (SMFs) exposure induces plasma membrane perturbation, including the rearrangement of lipid rafts, we investigated whether SMF could increase the amount of AgNPs able to pass the peripheral blood lymphocytes (PBLs) plasma membrane. To this purpose, the effect of 6-mT SMF exposure on the redistribution of two main lipid raft components (i.e., disialoganglioside GD3, cholesterol) and on AgNPs uptake efficiency was investigated. Results showed that 6 mT SMF: (i) induces a time-dependent GD3 and cholesterol redistribution in plasma membrane lipid rafts and modulates gene expression of ATP-binding cassette transporter A1 (ABCA1), (ii) increases reactive oxygen species (ROS) production and lipid peroxidation, (iii) does not induce cell death and (iv) induces lipid rafts rearrangement, that, in turn, favors the uptake of AgNPs. Thus, it derives that SMF exposure could be exploited to enhance the internalization of NPs-loaded therapeutic or diagnostic molecules.

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