GEO series

The anti-inflammatory nature of HDL in macrophages is mediated by ATF3

GSE44034 Mus musculus (mouse) Expression microarray 60 samples Submitted 2013/12/08 Platform GPL6887

At a glance

Expression microarray · mouse · 60 samples

What it is: Expression microarrayGene activity read on a chip (the older technology that RNA-seq replaced).
Organism: Mus musculus (mouse)
Samples: 60 samples: 60 samples, each with a distinct title — no replicated groupsGroups are read from the sample names, not from the paper. Check the list below.
Data you can get: A processed expression table (series matrix) and the array files, from NCBI.

Summary (written by the submitters)

Elevated plasma levels of High Density Lipoprotein (HDL) are associated with decreased risk of cardiovascular disease (CVD). The protective role of HDL in atherosclerosis has been attributed primarily to its ability to remove excess cholesterol from lipid-laden macrophages (foam cells) within the arterial walls. However, clinical trials that raise HDL cholesterol levels have failed to show a benefit casting doubts on our basic understanding of HDL function.

Read the full summary ↓

Atherosclerosis is a chronic inflammatory condition underlying CVD and driven in part by the recognition of metabolic danger signals by innate immune receptors on macrophages. A potential feature that could contribute to HDL’s protective effects in CVD could be HDL's anti-inflammatory nature, such as its ability to reduce endothelial cell activation. However, the molecular mechanisms by which HDL reduces inflammatory macrophage responses remain poorly understood and difficult to separate from its cholesterol depleting activity. Here we show that HDL protects against Toll like receptor (TLR)-induced inflammation both in vivo and in vitro under normocholesteremic conditions by suppressing the transcription of inflammatory cytokines in a manner independent of its ability to remove cellular cholesterol. We identify Activating Transcription Factor 3 (ATF3), a transcriptional repressor of the CREB family of basic leucine zipper transcription factors, as a HDL-inducible regulator of macrophage activation. HDL’s ability to down modulate TLR responses was severely compromised in ATF3-deficient cells demonstrating that ATF3 mediates HDL's anti-inflammatory effects and may explain the broad anti-inflammatory functions of HDL.

This dataset

Open GSE44034 in finder → Find more mouse microarray datasets →

Download · which file do I need?

Direct links to NCBI, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need.

All supplementary files ↗

3 · The original raw files

Whole study · RAW.tar

Everything the authors deposited as one archive (GSE44034_RAW.tar), including the raw array or instrument files. Can be large; the picker in step 2 takes just the samples you need.

Whole study · RAW.tar ↓

What the files usually look like: For arrays the series matrix is normally the normalised expression table you want; the raw array files (CEL and similar) are in the RAW.tar.

Also filed as BioProject PRJNA188404. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 24317040) ↗

Study design

60 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 60 sample titles: 60 distinct titles with little repetition. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study

GSM1077056 7166151005_A [HDL + CpG]
GSM1077060 7166151005_F [HDL]
GSM1077063 7911798003_C [Control]
GSM1077064 7911798003_D [CpG]
GSM1077065 7911798003_E [Control]
GSM1077066 7911798003_F [CpG]
GSM1077067 7911819006_A [HDL]
GSM1077068 7911819006_B [CpG]
GSM1077069 7911819006_C [HDL + CpG]
GSM1077070 7911819006_D [Control]
GSM1077071 7911819006_E [HDL]
GSM1077072 7911819006_F [HDL + CpG]
GSM1077074 8615616020_A [con]
GSM1077075 8615616020_B [HDL+CpG]
GSM1077076 8615616020_C [CpG]
GSM1077077 8615616020_D [con]
GSM1077078 8615616020_E [con]
GSM1077079 8615616020_F [HDL]
GSM1077080 8615616023_A [con]
GSM1077081 8615616023_B [HDL+P3C]
GSM1077082 8615616023_C [P3C]
GSM1077083 8615616023_D [HDL+P3C]
GSM1077084 8615616023_E [P3C]
GSM1077085 8615616023_F [con]
GSM1077086 8784129004_A [HDL]
GSM1077087 8784129004_B [HDL]
GSM1077088 8784129004_C [CpG]
GSM1077089 8784129004_D [CpG]
GSM1077090 8784129004_E [HDL+CpG]
GSM1077091 8784129004_F [HDL+CpG]
GSM1077092 8784129010_A [CpG]
GSM1077093 8784129010_B [HDL+CpG]
GSM1077094 8784129010_C [P3C]
GSM1077095 8784129010_D [HDL+P3C]
GSM1077096 8784129010_E [HDL+CpG]
GSM1077097 8784129010_F [P3C]
GSM1077098 8784129020_A [P3C]
GSM1077099 8784129020_B [HDL]
GSM1077100 8784129020_C [CpG]
GSM1077101 8784129020_D [HDL+CpG]

+ 20 more — browse all 60 samples with per-sample file links →

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