Do local anesthetics interact preferentially with membrane lipid rafts? Comparative interactivities with raft-like membranes

2010 ◽  
Vol 24 (4) ◽  
pp. 639-642 ◽  
Author(s):  
Hironori Tsuchiya ◽  
Takahiro Ueno ◽  
Maki Mizogami ◽  
Ko Takakura
Keyword(s):  
Lipid Rafts ◽  
Local Anesthetics ◽  
Membrane Lipid

scholarly journals Palmitic acid promotes resistin-induced insulin resistance and inflammation in SH-SY5Y human neuroblastoma

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hamza Amine ◽  
Yacir Benomar ◽  
Mohammed Taouis
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Palmitic Acid ◽  
Lipid Rafts ◽  
Acid Treatment ◽  
Protective Action ◽  
Saturated Fatty Acids ◽  
Membrane Lipid ◽  
Human Neuroblastoma ◽  
Peripheral Tissues

AbstractSaturated fatty acids such as palmitic acid promote inflammation and insulin resistance in peripheral tissues, contrasting with the protective action of polyunsaturated fatty acids such docosahexaenoic acid. Palmitic acid effects have been in part attributed to its potential action through Toll-like receptor 4. Beside, resistin, an adipokine, also promotes inflammation and insulin resistance via TLR4. In the brain, palmitic acid and resistin trigger neuroinflammation and insulin resistance, but their link at the neuronal level is unknown. Using human SH-SY5Yneuroblastoma cell line we show that palmitic acid treatment impaired insulin-dependent Akt and Erk phosphorylation whereas DHA preserved insulin action. Palmitic acid up-regulated TLR4 as well as pro-inflammatory cytokines IL6 and TNFα contrasting with DHA effect. Similarly to palmitic acid, resistin treatment induced the up-regulation of IL6 and TNFα as well as NFκB activation. Importantly, palmitic acid potentiated the resistin-dependent NFkB activation whereas DHA abolished it. The recruitment of TLR4 to membrane lipid rafts was increased by palmitic acid treatment; this is concomitant with the augmentation of resistin-induced TLR4/MYD88/TIRAP complex formation mandatory for TLR4 signaling. In conclusion, palmitic acid increased TLR4 expression promoting resistin signaling through TLR4 up-regulation and its recruitment to membrane lipid rafts.

1P-0227 Apolipoprotein A-1 interaction with plasma membrane lipid rafts controls cholesterol export from macrophages

2003 ◽  
Vol 4 (2) ◽  
pp. 69 ◽  
Author(s):  
W. Jessup ◽  
K. Gaus ◽  
L. Kritharides ◽  
A. Boettcher ◽  
W. Drobnik ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Lipid Rafts ◽  
Membrane Lipid ◽  
Apolipoprotein A ◽  
Plasma Membrane Lipid

Chapter 13 The Pivotal Role of Cholesterol and Membrane Lipid Rafts in the Ca

2016 ◽  
pp. 333-342
Author(s):  
Ying Zhang ◽  
Hiroko Kishi ◽  
Katsuko Kajiya ◽  
Tomoka Morita ◽  
Sei Kobayashi
Keyword(s):  
Lipid Rafts ◽  
Membrane Lipid ◽  
Pivotal Role

scholarly journals Interaction of drugs with lipid raft membrane domains as a possible target

2020 ◽  
Vol 14 (1) ◽  
pp. 34-47
Author(s):  
Hironori Tsuchiya ◽  
Maki Mizogami
Keyword(s):  
Membrane Fluidity ◽  
Lipid Rafts ◽  
Lipid Raft ◽  
Plasma Membranes ◽  
Cellular Membrane ◽  
Membrane Lipid ◽  
Membrane Domains ◽  
Functional Protein ◽  
Lipid Complex ◽  
Physicochemical Changes

Introduction: Plasma membranes are not the homogeneous bilayers of uniformly distributed lipids but the lipid complex with laterally separated lipid raft membrane domains, which provide receptor, ion channel and enzyme proteins with a platform. The aim of this article is to review the mechanistic interaction of drugs with membrane lipid rafts and address the question whether drugs induce physicochemical changes in raft-constituting and raft-surrounding membranes. Methods: Literature searches of PubMed/MEDLINE and Google Scholar databases from 2000 to 2020 were conducted to include articles published in English in internationally recognized journals. Collected articles were independently reviewed by title, abstract and text for relevance. Results: The literature search indicated that pharmacologically diverse drugs interact with raft model membranes and cellular membrane lipid rafts. They could physicochemically modify functional protein-localizing membrane lipid rafts and the membranes surrounding such domains, affecting the raft organizational integrity with the resultant exhibition of pharmacological activity. Raft-acting drugs were characterized as ones to decrease membrane fluidity, induce liquid-ordered phase or order plasma membranes, leading to lipid raft formation; and ones to increase membrane fluidity, induce liquid-disordered phase or reduce phase transition temperature, leading to lipid raft disruption. Conclusion: Targeting lipid raft membrane domains would open a new way for drug design and development. Since angiotensin-converting enzyme 2 receptors which are a cell-specific target of and responsible for the cellular entry of novel coronavirus are localized in lipid rafts, agents that specifically disrupt the relevant rafts may be a drug against coronavirus disease 2019.

Fluorescent Labeling of Membrane Lipid Rafts

2011 ◽  
Vol 2011 (5) ◽  
pp. pdb.prot5625-pdb.prot5625 ◽  
Author(s):  
B. Chazotte
Keyword(s):  
Lipid Rafts ◽  
Membrane Lipid ◽  
Fluorescent Labeling

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.

scholarly journals Activation of integrin α5 mediated by flow requires its translocation to membrane lipid rafts in vascular endothelial cells

2016 ◽  
Vol 113 (3) ◽  
pp. 769-774 ◽  
Author(s):  
Xiaoli Sun ◽  
Yi Fu ◽  
Mingxia Gu ◽  
Lu Zhang ◽  
Dan Li ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Lipid Rafts ◽  
Lipid Raft ◽  
Density Lipoprotein ◽  
Membrane Lipid ◽  
Local Flow ◽  
Atherosclerotic Lesions ◽  
Integrin Α5

Local flow patterns determine the uneven distribution of atherosclerotic lesions. Membrane lipid rafts and integrins are crucial for shear stress-regulated endothelial function. In this study, we investigate the role of lipid rafts and integrin α5 in regulating the inflammatory response in endothelial cells (ECs) under atheroprone versus atheroprotective flow. Lipid raft proteins were isolated from ECs exposed to oscillatory shear stress (OS) or pulsatile shear stress, and then analyzed by quantitative proteomics. Among 396 proteins redistributed in lipid rafts, integrin α5 was the most significantly elevated in lipid rafts under OS. In addition, OS increased the level of activated integrin α5 in lipid rafts through the regulation of membrane cholesterol and fluidity. Disruption of F-actin-based cytoskeleton and knockdown of caveolin-1 prevented the OS-induced integrin α5 translocation and activation. In vivo, integrin α5 activation and EC dysfunction were observed in the atheroprone areas of low-density lipoprotein receptor-deficient (Ldlr−/−) mice, and knockdown of integrin α5 markedly attenuated EC dysfunction in partially ligated carotid arteries. Consistent with these findings, mice with haploinsufficency of integrin α5 exhibited a reduction of atherosclerotic lesions in the regions under atheroprone flow. The present study has revealed an integrin- and membrane lipid raft-dependent mechanotransduction mechanism by which atheroprone flow causes endothelial dysfunction.

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