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Alteration of lipid homeostasis by hydroxypropyl cyclodextrin improves amiodarone-induced alveolar cell disorder

ABSTRACT: Alteration of lipid homeostasis by hydroxypropyl cyclodextrin improves amiodarone-induced alveolar cell disorder

PROVIDER: PRJNA611495 | ENA |

REPOSITORIES: ENA

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Alteration of lipid homeostasis by hydroxypropyl cyclodextrin improves amiodarone-induced alveolar cell disorder

Project description:We developed LB cells overexpressing ABCA3, SFTPB, SFTPC, and SFTPD in A549 cells. Using LB cells in high content screening, we identified HPbCD. HPbCD improved amiodarone-induced LB abnormality in iPS cell-derived alveolar organoids.

2021-02-20 | GSE146612 | GEO

Hydroxypropyl-β-cyclodextrin spikes local inflammation that induces Th2 and Tfh responses to the coadministered antigen

Project description:Gene expression data from mouse organs after hydroxypropyl-β-cyclodextrin injection Cyclodextrins are commonly used as a safe excipient to enhance the solubility and bioavailability of hydrophobic pharmaceutical agents. In this study, we reprofiled hydroxypropyl-β-cyclodextrin (HP-β-CD) as a vaccine adjuvant, and found that it acts as a potent and unique adjuvant.

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Hydroxypropyl-Î²-cyclodextrin spikes local inflammation that induces Th2 and Tfh responses to the coadministered antigen

Project description:Gene expression data from mouse organs after hydroxypropyl-Î²-cyclodextrin injection Cyclodextrins are commonly used as a safe excipient to enhance the solubility and bioavailability of hydrophobic pharmaceutical agents. In this study, we reprofiled hydroxypropyl-Î²-cyclodextrin (HP-Î²-CD) as a vaccine adjuvant, and found that it acts as a potent and unique adjuvant. C57BL/6J mice (6 week old, male, n = 3) were injected i.d. or i.p. with a total volume of 200 micro liter of 30% HP-Î²-CD in PBS. The vehicle-control mice (n = 3) were injected with the same volume of PBS. After 6 h, the inguinal LNs, Liver, and Spleen were removed (within one hour for all samples) and global gene expression was obtained by Affymetrix GeneChip.

2015-02-15 | E-GEOD-63332 | biostudies-arrayexpress

Cyclodextrin treatment leads to atherosclerosis regression by dissolution of cholesterol crystals and LXR activation

Project description:Atherosclerosis is an inflammatory disease linked to elevated blood cholesterol levels. Since cholesterol retention and cholesterol crystals in arterial walls are key pathogenetic factors for atherogenesis, we assessed the therapeutic potential of increasing cholesterol solubility in vivo. Here we show that treatment of murine atherosclerosis with the cyclic oligosaccharide 2-hydroxypropyl-β-cyclodextrin (CD), a compound that solubilizes lipophilic substances, reduced atherosclerotic plaque size, cholesterol crystal (CC) load and promoted plaque regression even under continuing Western diet. CD solubilized CC and promoted cholesterylester and oxysterol production in macrophages leading to liver X receptor-mediated transcriptional reprogramming with increased cholesterol efflux and decreased inflammation. CD treatment may thus be used to increase cholesterol solubility and clearance to prevent or treat atherosclerosis.

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mRNA expression data from keratinocytes with disorganized lipid raft structures (by cholesterol depletion by methyl-beta-cyclodextrin)

Project description:Lipid rafts are cholesterol-rich cell signaling platforms and their physiological role can be explored by cholesterol depletion. To dress a global picture of transcriptional changes ongoing after lipid raft disruption, we performed whole-genome expression profiling in epidermal keratinocytes, a cell type which synthesizes its cholesterol in situ. We used microarrays to identify transcriptional changes in gene expression of cholesterol-depleted keratinocytes. Cholesterol depletion by methyl-beta-cyclodextrin disrupts the organization of lipid rafts, which are cholesterol- and sphingolipid-rich membrane microdomains. Transcript levels were measured in autocrine confluent cultures of normal human epidermal keratinocytes were either left untreated (Ctrl), cholesterol-depleted for 1h with 7.5mM methyl-beta-cyclodextrin (MBCD), or mock cholesterol-depleted for 1h with 7.5mM cholesterol-charged methyl-beta-cyclodextrin complexes (MBCD/chol) (Mock cholesterol depletion is a suppementary negative control as this treatment does not extract cholesterol from cell membranes). Samples are analysed either immediately after the treatment (R0h) or after recovery times of 1h (R1h) respectively 8h (R8h). in total 9 samples are analysed and no replicates are performed.

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Transcriptome of 2-hydroxypropyl-beta-cyclodextrin treatment in Niemann-Pick disease type C1

Project description:Transcriptome of 2-hydroxypropyl-beta-cyclodextrin treatment in Niemann-Pick disease type C1

| PRJNA717336 | ENA

Transcriptome of 2-hydroxypropyl-beta-cyclodextrin treatment in Niemann-Pick disease type C1

Project description:Transcriptome of 2-hydroxypropyl-beta-cyclodextrin treatment in Niemann-Pick disease type C1

| PRJNA717337 | ENA

Cyclodextrin promotes atherosclerosis regression via LXR activation (II)

Project description:Atherosclerosis is an inflammatory disease linked to elevated blood cholesterol levels. Despite ongoing advances in the prevention and treatment of atherosclerosis 1, cardiovascular disease remains the leading cause of death worldwide 2. Continuous retention of apolipoprotein B-containing lipoproteins in the subendothelial space causes a local overabundance of free cholesterol. Since cholesterol accumulation and deposition of cholesterol crystals (CCs) triggers a complex inflammatory response 3 4, we tested the therapeutic potential of increasing cholesterol solubility in experimental atherogenesis. Here we show that treatment of murine atherosclerosis with the cyclic oligosaccharide 2-hydroxypropyl-β-cyclodextrin (CD), a compound that solubilizes lipophilic substances, reduced atherosclerotic plaque size, cholesterol crystal load and promoted plaque regression even under continuing Western diet. CD solubilized CCs and promoted cholesterylester and oxysterol production in macrophages leading to liver X receptor (LXR)-mediated transcriptional reprogramming. CD increased cholesterol efflux from macrophages and substantially augmented reverse cholesterol transport in vivo. Furthermore, CD reduced proinflammatory cytokines in vivo and decreased macrophage responsiveness towards TLR and inflammasome activation. Since CD treatment in humans is safe and CD beneficially affects key pathogenetic factors in atherogenesis it may thus be used clinically to prevent or treat human atherosclerosis .

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Cyclodextrin promotes atherosclerosis regression via LXR activation (I)

2016-05-06 | GSE67011 | GEO

Transcription profiling time series of human HeLa cells cultivated while sterol depleted from the medium

Project description:The aim of the experiment was to identify novel genes with relevance to cellular cholesterol metabolism. HeLa cells were cultivated while sterol was depleted from the medium by applying 2-Hydroxypropyl-cyclodextrin. RNA for expression profiling was isolated 3h, 4.5h and 6h after depletion.

2008-12-17 | E-TABM-599 | biostudies-arrayexpress

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