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SRNA sequencing of miRNAs in primary human islets

ABSTRACT: miRNAs are exported to high density lipoproteins (HDL). This study aimed to understand what miRNAs are present in primary human islets from 1 donor

ORGANISM(S): Homo sapiens

PROVIDER: GSE125137 | GEO | 2019/01/16

REPOSITORIES: GEO

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sRNA sequencing of miRNAs exported to HDL from primary human islets

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MicroRNAs are Transported in Plasma and Delivered to Recipient Cells by High-Density Lipoproteins

Project description:This SuperSeries is composed of the following subset Series: GSE25108: MicroRNAs are Transported in Plasma and Delivered to Recipient Cells by High-Density Lipoproteins (Human HDL miRNA Signatures) GSE25110: MicroRNAs are Transported in Plasma and Delivered to Recipient Cells by High-Density Lipoproteins (Human HDL and Exosome miRNA Signatures) GSE25149: MicroRNAs are Transported in Plasma and Delivered to Recipient Cells by High-Density Lipoproteins (Human exosome, LDL, and HDL miRNA Signatures) GSE25150: MicroRNAs are Transported in Plasma and Delivered to Recipient Cells by High-Density Lipoproteins (Mouse HDL signatures from WT and LDLR-/- high fat diet) GSE25311: MicroRNAs are Transported in Plasma and Delivered to Recipient Cells by High-Density Lipoproteins (HG-U133 2.0) GSE25424: MicroRNAs are Transported in Plasma and Delivered to Recipient Cells by High-Density Lipoproteins (microRNA signatures retrieved from rHDL injected into WT, ApoE-/- chow, ApoE-/-high fat diet) Refer to individual Series

2011-04-03 | E-GEOD-25425 | biostudies-arrayexpress

Transcription profiling of human pancreatic beta cells reveals the involvement of 4E-BP1 in the protection induced by HDLs

Project description:High-density lipoproteins (HDLs) protect pancreatic Î² cells against apoptosis. This property might be related to the increased risk to develop diabetes in patients with low HDL blood levels. However, the mechanisms by which HDLs protect Î² cells are poorly characterized. Here we use a transcriptomic approach to identify genes differentially modulated by HDLs in Î² cells subjected to apoptotic stimuli. Experiment Overall Design: Tested conditions on beta-TC3 cells for 6h (in triplicates for each condition; GSK3 and GSK4 indicate two independent HDL preparations): Experiment Overall Design: Complete Medium + Vehicle [V] Experiment Overall Design: Complete Medium + HDL (prep. HDL GSK3 or HDL GSK4) [HDL] Experiment Overall Design: Starvation medium + Vehicle [V.S] Experiment Overall Design: Starvation medium + HDL (prep. HDL GSK3 or HDL GSK4) [HDL.S]

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High density lipoproteins – a therapeutic target for age-related macular degeneration

Project description:We analyzed Apolipoprotein A-1 (ApoA-1) containing lipoproteins isolated from Bruch’s membrane (BrM) of elderly human donor eyes and found a unique proteome, quite different from HDL isolated from donor plasma of the same individuals. The most striking difference is higher concentrations of ApoB and ApoE, which bind to glycosaminoglycans (GAGs). We hypothesize that this interaction promotes lipoprotein deposition onto BrM GAGs, initiating downstream effects that contribute to RPE dysfunction/death. We tested this hypothesis using two therapeutic strategies to alter the lipoprotein/protein profile of these extracellular deposits. First, we used short, heparan sulfate oligosaccharides to remove lipoproteins already deposited in both the extracellular matrix of RPE cells and in aged, donor BrM tissue. Second, we used an ApoA-1 mimetic, 5A peptide, which modulates the relative amounts of cholesterol and ApoA-1, ApoB, and ApoE secreted both apically and basolaterally from primary porcine RPE cells. Significantly, the 5A peptide altered the proteomic profile of circulating HDL and ameliorated some of the potentially harmful changes in protein composition seen with a high fat, high cholesterol diet in a mouse model of AMD. Together, these results indicate that HDL interactions with BrM represent a viable target to slow AMD progression in humans

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