Relevant bibliographies by topics / Decoy liposomes

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  2. Dissertations / Theses

Academic literature on the topic 'Decoy liposomes'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 February 2022

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Journal articles on the topic "Decoy liposomes"

1

Ayllon, Marcelo, Gamid Abatchev, Andrew Bogard, Rosey Whiting, Sarah E. Hobdey, and Daniel Fologea. "Liposomes Prevent In Vitro Hemolysis Induced by Streptolysin O and Lysenin." Membranes 11, no. 5 (May 18, 2021): 364. http://dx.doi.org/10.3390/membranes11050364.

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The need for alternatives to antibiotics in the fight against infectious diseases has inspired scientists to focus on antivirulence factors instead of the microorganisms themselves. In this respect, prior work indicates that tiny, enclosed bilayer lipid membranes (liposomes) have the potential to compete with cellular targets for toxin binding, hence preventing their biological attack and aiding with their clearance. The effectiveness of liposomes as decoy targets depends on their availability in the host and how rapidly they are cleared from the circulation. Although liposome PEGylation may improve their circulation time, little is known about how such a modification influences their interactions with antivirulence factors. To fill this gap in knowledge, we investigated regular and long-circulating liposomes for their ability to prevent in vitro red blood cell hemolysis induced by two potent lytic toxins, lysenin and streptolysin O. Our explorations indicate that both regular and long-circulating liposomes are capable of similarly preventing lysis induced by streptolysin O. In contrast, PEGylation reduced the effectiveness against lysenin-induced hemolysis and altered binding dynamics. These results suggest that toxin removal by long-circulating liposomes is feasible, yet dependent on the particular virulence factor under scrutiny.
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Hendricks, Gabriel L., Lourdes Velazquez, Serena Pham, Natasha Qaisar, James C. Delaney, Karthik Viswanathan, Leila Albers, et al. "Heparin octasaccharide decoy liposomes inhibit replication of multiple viruses." Antiviral Research 116 (April 2015): 34–44. http://dx.doi.org/10.1016/j.antiviral.2015.01.008.

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Buchanan, Kyle D., Shao-Ling Huang, Hyunggun Kim, David D. McPherson, and Robert C. MacDonald. "Encapsulation of NF-κB decoy oligonucleotides within echogenic liposomes and ultrasound-triggered release." Journal of Controlled Release 141, no. 2 (January 2010): 193–98. http://dx.doi.org/10.1016/j.jconrel.2009.09.017.

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Tomita, Naruya, Masatsugu Horiuchi, Sawako Tomita, Gary H. Gibbons, John Y. S. Kim, Dana Baran, and Victor J. Dzau. "An oligonucleotide decoy for transcription factor E2F inhibits mesangial cell proliferation in vitro." American Journal of Physiology-Renal Physiology 275, no. 2 (August 1, 1998): F278—F284. http://dx.doi.org/10.1152/ajprenal.1998.275.2.f278.

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The transcription factor E2F controls expression of several genes involved in cell proliferation including c- myc, c- myb, proliferating cell nuclear antigen (PCNA), and cdk2 kinase. Having established that both PCNA and cdk2 kinase are induced in rat mesangial cells (MC) by serum stimulation, we attempted to inhibit MC proliferation in vitro by transfecting these cells with cationic liposomes containing a synthetic double-stranded oligodeoxynucleotide (ODN) with high affinity for E2F. Using a gel mobility shift assay, we detected increased specific binding of E2F in MC following serum stimulation. This binding was completely inhibited by preincubation of MC nuclear extracts with the double-stranded ODN with high affinity for E2F but not by preincubation with a missense ODN containing two point mutations. MC were also transfected with a luciferase reporter gene construct containing three E2F binding sites. Luciferase activity was enhanced by serum stimulation of MC, and this effect was specifically abolished by cotransfection of MC with E2F decoy ODN. Furthermore, RT-PCR analysis revealed that serum-induced upregulation of PCNA and cdk2 kinase gene expression was inhibited by E2F decoy ODN transfection but not by transfection of missense ODN. These changes in gene expression were paralleled by a reduction in PCNA and cdk2 kinase protein expression in E2F decoy ODN transfected cells. MC number increased following serum stimulation. This effect was blunted by transfection with E2F decoy ODN but not by transfection of missense ODN. These data suggest that the transcription factor E2F plays a crucial role in the regulation of MC proliferation and that this factor can be successfully targeted to inhibit MC cell cycle progression.
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Buchanan, Kyle D., ShaoLing Huang, Susan D. Tiukinhoy-Laing, David D. McPherson, and Robert C. MacDonald. "1024. Encapsulation of the NF-kB Decoy Oligonucleotide in Echogenic Liposomes and Its Ultrasound-Triggered Release." Molecular Therapy 13 (2006): S394. http://dx.doi.org/10.1016/j.ymthe.2006.08.1119.

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Borgatti, Monica, Laura Breda, Rita Cortesi, Claudio Nastruzzi, Alessandra Romanelli, Michele Saviano, Nicoletta Bianchi, Carlo Mischiati, Carlo Pedone, and Roberto Gambari. "Cationic liposomes as delivery systems for double-stranded PNA–DNA chimeras exhibiting decoy activity against NF-κB transcription factors." Biochemical Pharmacology 64, no. 4 (August 2002): 609–16. http://dx.doi.org/10.1016/s0006-2952(02)01188-7.

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Kraus, Damian, M. Edward Medof, and Carolyn Mold. "Complementary Recognition of Alternative Pathway Activators by Decay-Accelerating Factor and Factor H." Infection and Immunity 66, no. 2 (February 1, 1998): 399–405. http://dx.doi.org/10.1128/iai.66.2.399-405.1998.

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ABSTRACT The alternative complement pathway (ACP) functions as a surveillance mechanism by which microorganisms are opsonized with C3b in the absence of specific antibodies. The effectiveness of the ACP relies on its ability to distinguish self from non-self. This recognition function is mediated by C3 regulatory proteins including serum factor H, membrane cofactor protein (MCP), and membrane decay-accelerating factor (DAF). H activity against bound C3b can be increased by host components such as sialic acid and decreased by microbial polysaccharides. DAF and MCP may also recognize cell surface changes such as the presence of viral glycoproteins, since some virus-infected and tumor cells activate the ACP. In the present study, liposomes containing wild-type and mutant Salmonella minnesota lipopolysaccharide (LPS) were tested for ACP activation in serum. LPS-containing liposomes with bound C3b were then tested for their susceptibility to C3 convertase regulation by H and membrane DAF and for the sensitivity of their bound C3b to the cofactor activity of H. The results indicate that while the shortest mutant, Re595 LPS, did not induce ACP activation, R7 LPS containing an additional disaccharide did. This activation was poorly regulated by DAF but was inhibited by H. The regulatory activity of H for liposome-bound C3b, however, decreased when LPS of greater polysaccharide size was present in the membrane. In contrast the ACP activation induced by the phospholipid phosphatidylethanolamine was effectively inhibited by DAF but only poorly inhibited by H.
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8

Pilch, Ewa, and Witold Musiał. "Selected Physicochemical Properties of Lyophilized Hydrogel with Liposomal Fraction of Calcium Dobesilate." Materials 11, no. 11 (October 31, 2018): 2143. http://dx.doi.org/10.3390/ma11112143.

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Lyophilization is the process of drying and improving the stability of various pharmaceutical preparations. In this work we evaluated the properties of 11 hydrophilic gels calcium dobesilate with liposomes based on soybean lecithin, subjected to the freeze-drying procedure. Liposomes were produced by using method thin lipid film. Lyophilization was carried out under conditions of temperature equal (−30 °C) and pressure 0.37 mbar. We evaluated the preparations with dynamic light scattering (DLS) method, optical microscopy and Fourier-transform infrared spectroscopy (FTIR). In this work we presented the average results for the particle diameter in the sample and PDI (polydispersity index) value for the samples that produced the results. When testing using the DLS method on a Malvern Zetaseizer, results for 7 samples were not obtained. Two of next four samples were characterized by an increased size of the liposome particle resulting from a lower concentration of ethanol compared to the rest of them. Three samples under the microscope did not show any differences. It was possible only to see single crystals probably of undissolved calcium dobesilate. Some clusters were observed in the 4 samples, and when they appeared they were very small. The aggregates and irregular liposomes present in the rest of the samples may have been formed due to the destabilizing activity of ethanol towards lipid membranes. In the FTIR spectrum for MC, the peak was observed at the wavenumber of ca. 2900 cm−1 and of about 1050 cm−1. In case of pure calcium dobesilate we observed low pick at the wavenumber of about 3400 cm−1. The spectrum has a low peak at the wavenumber of 1450 cm−1 and intense peaks ranging from approx. 1000 cm−1 to approx. 1200 cm−1. Decay of the lecithin peak in formulations with liposomes at 1725 cm−1 wavelength may indicate the occurrence of the hydrolysis reaction in the system. Probably there was a hydrolysis of the ester bond connecting the rest of the phosphoric acid and the choline with the glycerol residue.
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9

Gabrielska, Janina, and Jan Oszmiański. "Antioxidant Activity of Anthocyanin Glycoside Derivatives Evaluated by the Inhibition of Liposome Oxidation." Zeitschrift für Naturforschung C 60, no. 5-6 (June 1, 2005): 399–407. http://dx.doi.org/10.1515/znc-2005-5-606.

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Cyanidin-3-glycosides (arabinoside, rutinoside, galactoside and glucoside) and delphinidin- 3-rutinoside were examined for their ability to inhibit lipid peroxidation induced either by Fe(II) ions, UV irradiation or 2,2′-azobis(2-amidinopropane) dihydrochloride (AAPH) peroxyl radicals in a liposomal membrane system. The antioxidant abilities of anthocyanins were compared with a water-soluble tocopherol derivative, trolox. The antioxidant efficacies of these compounds were evaluated by their ability to inhibit the fluorescence intensity decay of the extrinsic probe 3-[p-(6-phenyl)-1,3,5,-hexatrienyl] phenylpropionic acid, caused by the free radicals generated during peroxidation. All the anthocyanins tested (at concentrations of 15-20 μm) exhibited higher antioxidant activities against Fe(II)-induced peroxidation than UV- and AAPH-induced peroxidation, suggesting that metal chelation may play an important role in determining the antioxidant potency of these compounds. It was also found that delphinidin-3-rutinoside had a higher antioxidant activity against Fe(II)-induced liposome oxidation than cyanidin-3-rutinoside, which indicates an important role of the OH group in the B ring of delphinidin-3-rutinoside in its antioxidant action. The antioxidant activity of all the anthocyanins studied was higher than that of trolox in the case of Fe(II)-induced liposome oxidation and was comparable with the action of trolox in the case of UV- and AAPHinduced liposome membrane oxidation.
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10

Ramasamy, Thiruganesh, Xucai Chen, Bin Qin, Daniel E. Johnson, Jennifer R. Grandis, and Flordeliza S. Villanueva. "STAT3 decoy oligonucleotide-carrying microbubbles with pulsed ultrasound for enhanced therapeutic effect in head and neck tumors." PLOS ONE 15, no. 11 (November 18, 2020): e0242264. http://dx.doi.org/10.1371/journal.pone.0242264.

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Signal transducer and activator of transcription-3 (STAT3) is an oncogenic transcription factor implicated in carcinogenesis, tumor progression, and drug resistance in head and neck squamous cell carcinoma (HNSCC). A decoy oligonucleotide targeting STAT3 offers a promising anti-tumor strategy, but achieving targeted tumor delivery of the decoy with systemic administration poses a significant challenge. We previously showed the potential for STAT3 decoy-loaded microbubbles, in conjunction with ultrasound targeted microbubble cavitation (UTMC), to decrease tumor growth in murine squamous cell carcinoma. As a next step towards clinical translation, we sought to determine the anti-tumor efficacy of our STAT3 decoy delivery platform against human HNSCC and the effect of higher STAT3 decoy microbubble loading on tumor cell inhibition. STAT3 decoy was loaded on cationic lipid microbubbles (STAT3-MB) or loaded on liposome-conjugated lipid microbubbles to form STAT3-loaded liposome-microbubble complexes (STAT3-LPX). UTMC treatment efficacy with these two formulations was evaluated in vitro using viability and apoptosis assays in CAL33 (human HNSCC) cells. Anti-cancer efficacy in vivo was performed in a CAL33 tumor murine xenograft model. UTMC with STAT3-MB caused significantly lower CAL33 cell viability compared to UTMC with STAT3-LPX (56.8±8.4% vs 84.5±8.8%, respectively, p<0.05). In vivo, UTMC with STAT3-MB had strong anti-tumor effects, with significantly less tumor burden and greater survival compared to that of UTMC with microbubbles loaded with a mutant control decoy and untreated control groups (p<0.05). UTMC with STAT3 decoy-loaded microbubbles significantly decreases human HNSSC tumor progression. These data set the stage for clinical translation of our microbubble platform as an imaged-guided, targeted delivery strategy for STAT3 decoy, or other nucleotide-based therapeutics, in human cancer treatment.
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Dissertations / Theses on the topic "Decoy liposomes"

1

Hendricks, Gabriel L. "Modulating Influenza and Heparin Binding Viruses’ Pathogenesis with Extrinsic Receptor Decoy Liposomes: A Dissertation." eScholarship@UMMS, 2013. http://escholarship.umassmed.edu/gsbs_diss/674.

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Influenza is a severe disease in humans and animals, causing upwards of 40,000 deaths every year in America alone. Influenza A virus (IAV) also causes periodic pandemics every 10 to 50 years, killing millions of people. Despite this, very few effective therapies are available. All strains of IAV are prone to developing resistance to antibodies due to the high mutation rate in the viral genome. Because of this mutation rate, a yearly vaccine must be generated before every flu season, and efficacy varies year to year. IAV has also mutated to escape several of the clinically-approved small molecule inhibitors. A therapeutic agent that targets a highly conserved region of the virus could bypass resistance and also be effective against multiple strains of IAV. IAV attachment is mediated by many individually weak hemagglutinin–sialic acid interactions that all together make a strong attachment to a host cell. Polymerized sialic acid analogs can recreate these interactions and block infection. However, they are not ideal therapeutics due to solubility issues and in vivo toxicity. We used liposomes as a novel means for delivery of the sialic acid-containing glycan, sialylneolacto-N-tetraose c (LSTc). LSTcbearing decoy liposomes form multivalent, polymer-like interactions with IAV. Decoy liposomes competitively bind IAV in hemagglutination inhibition assays and inhibit infection of target cells in a dose-dependent manner. LSTc decoy liposomes co-localize with IAV, while control liposomes do not. Inhibition is specific, as inhibition of Sendai virus and respiratory syncytial virus is not observed. In contrast, monovalent LSTc does not bind IAV or inhibit infectivity. LSTc decoy liposomes prevent the spread of IAV during multiple rounds of replication in vitro and extend survival of mice challenged with a lethal dose of virus. Considering the conservation of the hemagglutinin binding pocket and the ability of decoy liposomes to form high-avidity interactions with IAV hemagglutinin, our decoy liposomes have potential as a new therapeutic agent against emerging strains.
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