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Germline deletion of Krüppel-like factor 14 does not increase risk of diet-induced metabolic syndrome in male C57BL/6 mice

ABSTRACT: The transcription factor Krüppel-like factor 14 (KLF14) has been associated with type 2 diabetes and high-density lipoprotein-cholesterol (HDL-C) through genome-wide association studies. The mechanistic underpinnings of KLF14's control of metabolic processes remain largely unknown. We studied the physiological roles of KLF14 in a knockout (KO) mouse model.

ORGANISM(S): Mus musculus

PROVIDER: GSE172090 | GEO | 2021/04/15

REPOSITORIES: GEO

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Germline deletion of Krüppel-like factor 14 does not increase risk of diet-induced metabolic syndrome in male C57BL/6 mice

Project description:Germline deletion of Krüppel-like factor 14 does not increase risk of diet-induced metabolic syndrome in male C57BL/6 mice

| PRJNA721979 | ENA

Structure dynamics of ApoA-I amyloidogenic variants in small HDL increase their ability to mediate cholesterol efflux

Project description:Specific mutations in Apolipoprotein A-I (ApoA-I) of high-density lipoprotein (HDL) are responsible for a late-onset systemic amyloidosis. Carriers do not exhibit increased cardiovascular disease risk despite reduced levels of ApoA-I/ HDL-cholesterol. To explain this paradox, we show that the HDL particle profile of L75P and L174S patients presents a higher relative abundance of the 8.4 nm vs 9.6 nm particles, and that serum from patients, as well as reconstituted 8.4 and 9.6 nm HDL particles (rHDL), possess increased capacity to catalyze cholesterol efflux from macrophages. Synchrotron radiation circular dichroism and hydrogen-deuterium exchange revealed that the variants in 8.4 nm rHDL have altered secondary structure composition and display a more flexible binding to lipids compared to their native counterpart. The reduced HDL-cholesterol levels of patients carrying ApoA-I amyloidogenic variants are thus balanced by higher proportion of small, dense HDL particles and better cholesterol efflux due to altered, region-specific protein structure dynamics.

2020-11-20 | PXD021266 | Pride

Germline deletion of Kruppel-like factor 14 does not increase risk of diet induced metabolic syndrome in male C57BL/6 mice.

Project description:ObjectiveThe transcription factor Krüppel-like factor 14 (KLF14) has been associated with type 2 diabetes and high-density lipoprotein-cholesterol (HDL-C) through genome-wide association studies. The mechanistic underpinnings of KLF14's control of metabolic processes remain largely unknown. We studied the physiological roles of KLF14 in a knockout (KO) mouse model.MethodsMale whole body Klf14 KO mice were fed a chow or high fat diet (HFD) and diet induced phenotypes were analyzed. Additionally, tissue-specific expression of Klf14 was determined using RT-PCR, RNA sequencing, immunoblotting and whole mount lacZ staining. Finally, the consequences of KLF14 loss-of-function were studied using RNA sequencing in tissues with relatively high Klf14 expression levels.ResultsKLF14 loss-of-function did not affect HFD-induced weight gain or insulin resistance. Fasting plasma concentrations of glucose, insulin, cholesterol, HDL-C and ApoA-I were also comparable between Klf14+/+ and Klf14-/- mice on chow and HFD. We found that in mice expression of Klf14 was the highest in the anterior pituitary (adenohypophysis), lower but detectable in white adipose tissue and undetectable in liver. Loss of KLF14 function impacted on the pituitary transcriptome with extracellular matrix organization as the primary affected pathway and a predicted link to glucocorticoid receptor signaling.ConclusionsWhole body loss of KLF14 function in male mice does not result in metabolic abnormalities as assessed under chow and HFD conditions. Mostly likely there is redundancy for the role of KLF14 in the mouse and a diverging function in humans.

| S-EPMC8607354 | biostudies-literature

MicroRNAs are Transported in Plasma and Delivered to Recipient Cells by High-Density Lipoproteins (HG-U133 2.0)

Project description:Circulating microRNAs (miRNA) are relatively stable in plasma and are a new class of disease biomarkers. Here we present evidence that human high-density lipoprotein (HDL) transports endogenous miRNAs and delivers them to recipient cells with functional targeting capabilities. Highly-purified fractions of human HDL contain small RNAs, and the HDL-miRNA profile from normal subjects is significantly different than familial hypercholesterolemia subjects. miRNAs were demonstrated to associate with both native and reconstituted HDL particles, and reconstituted HDL injected into mice retrieved distinct miRNA profiles from normal and atherogenic models. Cellular export of miRNAs to HDL was demonstrated to be regulated by neutral sphingomyelinase. HDL-mediated delivery of miRNAs to recipient cells was demonstrated to be scavenger receptor BI-dependent. Furthermore, HDL delivery of both exogenous and endogenous miRNAs resulted in the direct targeting of mRNA reporters. Notably, HDL-miRNA from atherosclerotic subjects induced differential gene expression, with significant loss of conserved mRNA targets in cultured hepatocytes. Collectively, these observations suggest that HDL participates in a novel mechanism of intercellular communication involving the transport and delivery of miRNAs. Gene expression changes in human Huh7 cells with familial hypercholesterolemia HDL treatment. Gene expression (mRNA) profiles in human Huh7 cells treated with normal HDL (n=3) or FH HDL (n=3) in lipoprotein-depleted serum (48h).

2011-03-24 | E-GEOD-25311 | biostudies-arrayexpress

Gene expression changes in Burkitt's lymphoma due to treatment with high density lipoprotein-like nanoparticles (HDL NP)

Project description:We report changes in gene expression in the Burkitt's lymphoma cell line Ramos, treated with high density lipoprotein-like nanoparticles (HDL NPs) for 48 hours, compared to saline (NT) and natural, human HDL treatment

2019-04-20 | GSE98028 | GEO

Transcription profiling of human native lipoprotein-stimulated THP-1 macrophages

Project description:We previously found that a native lipoprotein mix with a high VLDL+LDL/HDL ratio causes a global de novoDNA methylation in THP-1 macrophages. In the present experiment we assessed the consequences of global lipoprotein-induced de novo DNA methylation on global gene expression in the same cells. Moreover, we sought to use gene expression array data to measure RNA expression levels for candidate factors mediating the epigenetic effects of lipoproteins. Experiment Overall Design: Human native VLDL, LDL and HDL lipoproteins were isolated from buffy coats, fractionated by ultracentrifugation, stored at -80deg., desalted to PBS before usage and kept at 4deg. for a maximum of 7d. THP-1 monocytes were differentiated to macrophages, stimulated for 24h with a mix of 68.8mg/ml VLDL, 32.1mg/ml LDL, 91.1mg/ml HDL or unstimulated (control), in serum-free medium with 2% BSA. Three independently isolated lipoprotein samples were used in triplicate.

2008-06-16 | E-GEOD-9101 | biostudies-arrayexpress

Intestine-specific activation of LXR via low-dose oral administration of GW3965

Project description:Generation of high density lipoprotein (HDL) requires apoA1 and the cholesterol transporter ABCA1. Although the liver generates most HDL in blood, small intestines also can synthesize HDL. However, distinct functions for intestinal HDL are unknown. Here we designed intestine-specific activation of LXR via low-dose administration of GW3965, LXR agonist. The liver status was improved by therapeutics that elevated and depended upon intestinal HDL production via GW3965. Thus, protection of the liver from injury in response to gut-derived signals like LPS is a major function of intestinally synthesized HDL.

2021-10-06 | GSE167983 | GEO

PFOS and PFHxS decrease lipoprotein production

Project description:The effect of perfluoroalkyl sulfonates on lipoprotein metabolism was investigated in APOE*3-Leiden.CETP mice with a humanized lipoprotein profile. Perfluorohexane sulfonate and perfluorooctane sulfonate markedly reduced both plasma TG and TC by decreasing nonHDL-C and HDL-C accompanied by a reduction in apoAI. Mechanistic studies showed that these effects were mainly caused by impaired lipoprotein production.

2011-01-01 | GSE22940 | GEO

MicroRNAs are Transported in Plasma and Delivered to Recipient Cells by High-Density Lipoproteins (Human HDL miRNA Signatures)

Project description:Circulating microRNAs (miRNA) are relatively stable in plasma and are a new class of disease biomarkers. Here we present evidence that human high-density lipoprotein (HDL) transports endogenous miRNAs and delivers them to recipient cells with functional targeting capabilities. Highly-purified fractions of human HDL contain small RNAs, and the HDL-miRNA profile from normal subjects is significantly different than familial hypercholesterolemia subjects. miRNAs were demonstrated to associate with both native and reconstituted HDL particles, and reconstituted HDL injected into mice retrieved distinct miRNA profiles from normal and atherogenic models. Cellular export of miRNAs to HDL was demonstrated to be regulated by neutral sphingomyelinase. HDL-mediated delivery of miRNAs to recipient cells was demonstrated to be scavenger receptor BI-dependent. Furthermore, HDL delivery of both exogenous and endogenous miRNAs resulted in the direct targeting of mRNA reporters. Notably, HDL-miRNA from atherosclerotic subjects induced differential gene expression, with significant loss of conserved mRNA targets in cultured hepatocytes. Collectively, these observations suggest that HDL participates in a novel mechanism of intercellular communication involving the transport and delivery of miRNAs. Human HDL miRNA Signatures Profiled miRNA Signatures from N=6 Normal Human HDL; n=5 FH Human HDL

2011-03-23 | E-GEOD-25108 | biostudies-arrayexpress

MicroRNAs are Transported in Plasma and Delivered to Recipient Cells by High-Density Lipoproteins (Human HDL and Exosome miRNA Signatures)

Project description:Circulating microRNAs (miRNA) are relatively stable in plasma and are a new class of disease biomarkers. Here we present evidence that human high-density lipoprotein (HDL) transports endogenous miRNAs and delivers them to recipient cells with functional targeting capabilities. Highly-purified fractions of human HDL contain small RNAs, and the HDL-miRNA profile from normal subjects is significantly different than familial hypercholesterolemia subjects. miRNAs were demonstrated to associate with both native and reconstituted HDL particles, and reconstituted HDL injected into mice retrieved distinct miRNA profiles from normal and atherogenic models. Cellular export of miRNAs to HDL was demonstrated to be regulated by neutral sphingomyelinase. HDL-mediated delivery of miRNAs to recipient cells was demonstrated to be scavenger receptor BI-dependent. Furthermore, HDL delivery of both exogenous and endogenous miRNAs resulted in the direct targeting of mRNA reporters. Notably, HDL-miRNA from atherosclerotic subjects induced differential gene expression, with significant loss of conserved mRNA targets in cultured hepatocytes. Collectively, these observations suggest that HDL participates in a novel mechanism of intercellular communication involving the transport and delivery of miRNAs. Human HDL and Exosome miRNA Signatures Profiled miRNA signatures from HDL and exosome in matched subjects

2011-03-23 | E-GEOD-25110 | biostudies-arrayexpress

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