Targeting Cell Membrane Lipid Rafts by Stoichiometric Functionalization of Gold Nanoparticles with a Sphingolipid-Binding Domain Peptide

2015 ◽  
Vol 4 (6) ◽  
pp. 911-917 ◽  
Author(s):  
David Paramelle ◽  
Daniel Nieves ◽  
Benjamin Brun ◽  
Rachel S. Kraut ◽  
David G. Fernig
Keyword(s):  
Gold Nanoparticles ◽  
Cell Membrane ◽  
Lipid Rafts ◽  
Membrane Lipid ◽  
Binding Domain ◽  
Domain Peptide

scholarly journals Cell Membrane Lipid Rafts Mediate Caveolar Endocytosis of HIV-1 Tat Fusion Proteins

2003 ◽  
Vol 278 (36) ◽  
pp. 34141-34149 ◽  
Author(s):  
Antonio Fittipaldi ◽  
Aldo Ferrari ◽  
Monica Zoppé ◽  
Caterina Arcangeli ◽  
Vittorio Pellegrini ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Lipid Rafts ◽  
Fusion Proteins ◽  
Membrane Lipid ◽  
Tat Fusion Proteins ◽  
Hiv 1

scholarly journals Procyanidins can interact with Caco-2 cell membrane lipid rafts: Involvement of cholesterol

2013 ◽  
Vol 1828 (11) ◽  
pp. 2646-2653 ◽  
Author(s):  
Sandra V. Verstraeten ◽  
Grayson K. Jaggers ◽  
Cesar G. Fraga ◽  
Patricia I. Oteiza
Keyword(s):  
Cell Membrane ◽  
Lipid Rafts ◽  
Membrane Lipid

scholarly journals Further evidence that paroxysmal nocturnal haemoglobinuria is a disorder of defective cell membrane lipid rafts

2015 ◽  
Vol 19 (9) ◽  
pp. 2193-2201 ◽  
Author(s):  
Mariusz Z. Ratajczak ◽  
Sylwia Borkowska ◽  
Kasia Mierzejewska ◽  
Magda Kucia ◽  
Ewa Mendek-Czajkowska ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Lipid Rafts ◽  
Membrane Lipid ◽  
Paroxysmal Nocturnal Haemoglobinuria

scholarly journals A Retrospective Comparative Study of Sodium Fluoride (NaF-18)-PET/CT and Fluorocholine (F-18-CH) PET/CT in the Evaluation of Skeletal Metastases in Metastatic Prostate Cancer Using a Volumetric 3-D Radiomics Analysis

Diagnostics ◽  
2020 ◽  
Vol 11 (1) ◽  
pp. 17
Author(s):  
Kalevi Kairemo ◽  
S. Cheenu Kappadath ◽  
Timo Joensuu ◽  
Homer A. Macapinlac
Keyword(s):  
Prostate Cancer ◽  
Cell Membrane ◽  
Sodium Fluoride ◽  
Bone Mineralization ◽  
Membrane Lipid ◽  
Skeletal Metastases ◽  
Study Cohort ◽  
Skeletal Disease ◽  
Sclerotic Bone ◽  
Pet Ct

Bone metastases are common in prostate cancer (PCa). Fluorocholine-18 (FCH) and sodium fluoride-18 (NaF) have been used to assess PCa associated skeletal disease in thousands of patients by demonstrating different mechanism of uptake-cell membrane (lipid) synthesis and bone mineralization. Here, this difference is characterized quantitatively in detail. Our study cohort consisted of 12 patients with advanced disease (> 5 lesions) (M) and of five PCa patients with no skeletal disease (N). They had routine PET/CT with FCH and NaF on consecutive days. Skeletal regions in CT were used to co-register the two PET/CT scans. Bone 3-D volume of interest (VOI) was defined on the CT of PET with a threshold of HU > 150, and sclerotic/dense bone as HU > 600, respectively. Additional VOIs were defined on PET uptake with the threshold values on both FCH (SUV > 3.5) and NaF (SUV > 10). The pathologic skeletal volumes for each technique (CT, HU > 600), NaF (SUV > 10) and FCH (SUV > 3.5) were developed and analyzed. The skeletal VOIs varied from 5.03 L to 7.31 L, whereas sclerotic bone VOIs were from 0.88 L to 2.99 L. Total choline kinase (cell membrane synthesis) activity for FCH (TCA) varied from 0.008 to 4.85 [kg] in M group and from 0.0006 to 0.085 [kg] in N group. Total accelerated osteoblastic (bone demineralization) activity for NaF (TBA varied from 0.25 to 13.6 [kg] in M group and varied from 0.000 to 1.09 [kg] in N group. The sclerotic bone volume represented only 1.86 ± 1.71% of the pathologic FCH volume and 4.07 ± 3.21% of the pathologic NaF volume in M group, and only 0.08 ± 0.09% and 0.18 ± 0.19% in N group, respectively. Our results suggest that CT alone cannot be used for the assessment of the extent of active metastatic skeletal disease in PCa. NaF and FCH give complementary information about the activity of the skeletal disease, improving diagnosis and disease staging.

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

Time-Course of Changes in the Plasma–Membrane Lipid Bilayer and Cellular Ultrastructure Induced by Tumour Necrosis Factor-α in K 562 and Daudi Cells

1995 ◽  
Vol 23 (4) ◽  
pp. 254-263 ◽  
Author(s):  
M Marutaka ◽  
H Iwagaki ◽  
K Mizukawa ◽  
N Tanaka ◽  
K Orita
Keyword(s):  
Plasma Membrane ◽  
Cell Membrane ◽  
Membrane Fluidity ◽  
Time Course ◽  
Membrane Lipid ◽  
Plasma Membrane Lipid ◽  
Membrane Lipid Bilayer ◽  
Cell Membrane Fluidity ◽  
K 562 Cells ◽  
Factor Α

The time-course of changes in the plasma-membrane lipid bilayer induced by tumour necrosis factor-α (TNF) were investigated in cultured cells using spin-label electron-spin-resonance techniques. Treatment of K 562 cells, a human chronic myelocytic leukaemia cell line, in suspension culture with TNF for up to 6 h caused an initial increase in cell-membrane fluidity, which returned to the control level after 12 h of treatment. After 24 h of treatment, the cell-membrane fluidity had decreased and this decrease was maintained after 48 h of treatment. In Daudi cells, a human malignant lymphoma cell line, TNF, did not induce any changes in cell-membrane fluidity, indicating that the effect of TNF on membrane structure is cell-specific. The early and transient change in membrane fluidity in K 562 cells is probably related to signal generation, while the later, persistent change may reflect the phenotype of TNF-treated cells, in particular, changes in the plasma membrane-cytoplasmic complex. Histochemical electron microscopic studies indicated that the membrane fluidity changes induced by TNF have an ultrastructural correlate.

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