We generated a comprehensive dataset of RNA-Seq, ChiP-Seq (H3K27me3, H3K9me2, H3K27ac, H3K16ac, H3K9ac), proteomics and metabolomics on primary monocyte-derived macrophages from several donors. Now published in Nature, we hope the community can exploit this data further.
In our latest work published in Naturewe generated an extensive dataset using RNA-Seq, ChiP-Seq, metabolomics and proteomics on primary cells. We want to share this here in the Research Data Community as we think this is a very useful resource. On the whole, our study encompassed a novel mechanism of endocytosis, design of a new molecule to inhibit inflammation, the discovery that copper is implicated in the interconvertion of NAD(H), metabolomic and epigenetic characterisation and in vivo studies on inflammation. Because the paper is so rich, we think that an emphasis of the depth of the multiomics dataset is useful for people to read about.
Of course, according to Springer/ Nature policies, all the raw data and data are freely available and can be used by the scientific community.
Examples of metabolomics data used in the study. All raw data are freely available.
Importantly, we performed RNA-Seq on several donors and performed ChiP-Seq on 5 epigenetic marks: H3K27me3, H3K9me2, H3K27ac, H3K16ac, H3K9ac. This is quite unique, as often studies just look at one or two marks. However, we wanted to give a greater picture and this could now be used to look into the specific contribution of each of these activating and repressive marks and determine their exact contribution to gene expression.
Mitochondrial copper(II) regulates the epigenetic states and transcriptional programs of inflammatory macrophages. a, GO term analysis of upregulated genes in aMDM (n=10 donors). b, RNA-seq of MDM. Inflammatory gene signature highlighted in orange. Dashed line, adjusted p-value=0.05 (n=10 donors). c,RNA-seq of MDM. Iron-dependent demethylases and acetyl-transferases highlighted in blue and green, respectively. Dashed line, adjusted p-value=0.05 (n=10 donors). d, Scatter plot correlation of a representative donor of ChIP-seq read counts of histone marks in genes against RNA-seq of gene transcripts in MDM (n=10 donors). e, GO term analysis of genes in aMDM (n=10 donors) whose expression levels are downregulated upon treatment with LCC-12 (n=5 donors). f, RNA-seq of aMDM (n=10 donors) and MDM treated with LCC-12 during activation (n=5 donors). Inflammatory gene signature highlighted in orange. Dashed line, adjusted p-value=0.05. g, Scatter plot correlation of a representative donor of ChIP-seq read counts of histone marks in genes against RNA-seq of gene transcripts in aMDM (n=10 donors) and MDM treated with LCC-12 during activation (n=5 donors). h, RNA-seq of aMDM under CD44 knock out conditions. Representative of n=4 donors. Gating strategy see Supplementary Information. Inflammatory gene signature highlighted in orange. Dashed line, adjusted p-value=0.05. For a – c, e and f differential gene expression was assessed with the limma/voom framework. GO enrichment was assessed with the enrichGO method from clusterProfiler. P-values were corrected for multiple testing with the Benjamini-Hochberg procedure.
We hope these datasets will be useful for the community and are happy to work with anyone who would like to take this further.
Reference: Solier et al., A druggable copper-signalling pathway that drives inflammation, Nature, 2023, 617, 386–394, doi:10.1038/s41586-023-06017-4
Please sign in or register for FREE
If you are a registered user on Research Data at Springer Nature, please sign in
A weekly international journal publishing the finest peer-reviewed research in all fields of science and technology on the basis of its originality, importance, interdisciplinary interest, timeliness, accessibility, elegance and surprising conclusions.
We generated a comprehensive dataset of RNA-Seq, ChiP-Seq (H3K27me3, H3K9me2, H3K27ac, H3K16ac, H3K9ac), proteomics and metabolomics on primary monocyte-derived macrophages from several donors. Now published in Nature, we hope the community can exploit this data further.
This is a representation of how your post may appear on social media. The actual post will vary between social networks
We use cookies to ensure the functionality of our website, to personalize content and advertising, to provide social media features, and to analyze our traffic. If you allow us to do so, we also inform our social media, advertising and analysis partners about your use of our website. You can decide for yourself which categories you want to deny or allow. Please note that based on your settings not all functionalities of the site are available.
Customise your preferences for any tracking technology
The following allows you to customize your consent preferences for any tracking technology used
to help us achieve the features and activities described below. To learn more about how these trackers help us
and how they work, refer to the cookie policy. You may review and change your preferences at any time.
These trackers are used for activities that are strictly necessary to operate or deliver the service you requested from us and, therefore, do not require you to consent.
These trackers help us to provide a personalized user experience by improving the quality of your preference management options, and by enabling the interaction with external networks and platforms.
Nature
Please sign in or register for FREE
If you are a registered user on Research Data at Springer Nature, please sign in