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Transcriptome data and gene ontology analysis in human macrophages ingesting modified lipoproteins in the presence or absence of complement protein C1q.

ABSTRACT: We characterized the transcriptional effects of complement opsonization on foam cell formation in human monocyte-derived macrophages (HMDM). RNA-sequencing was used to identify the pathways modulated by complement protein C1q during HMDM ingestion of the atherogenic lipoproteins oxidized low density lipoprotein (oxLDL) and acetylated low density lipoprotein (acLDL). All raw data were submitted to the MIAME-compliant database Gene Expression Omnibus (accession number GEO: GSE80442; http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE80442). Data presented here include Venn diagram overviews of up- and down-regulated genes for each condition tested, gene ontology analyses of biological processes, molecular functions and cellular components and KEGG pathway analysis. Further investigation of the pathways modulated by C1q in HMDM during ingestion of atherogenic lipoproteins and their functional relevance are described in "Macrophage molecular signaling and inflammatory responses during ingestion of atherogenic lipoproteins are modulated by complement protein C1q" (M.M. Ho, A. Manughian-Peter, W.R. Spivia, A. Taylor, D.A. Fraser, 2016) [1].

SUBMITTER: Ho MM

PROVIDER: S-EPMC5035341 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature

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Transcriptome data and gene ontology analysis in human macrophages ingesting modified lipoproteins in the presence or absence of complement protein C1q.

Ho Minh-Minh MM Fraser Deborah A DA

Data in brief 20160914

We characterized the transcriptional effects of complement opsonization on foam cell formation in human monocyte-derived macrophages (HMDM). RNA-sequencing was used to identify the pathways modulated by complement protein C1q during HMDM ingestion of the atherogenic lipoproteins oxidized low density lipoprotein (oxLDL) and acetylated low density lipoprotein (acLDL). All raw data were submitted to the MIAME-compliant database Gene Expression Omnibus (accession number GEO: GSE80442; http://www.ncb ...[more]

PMID: 27699187

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Project description:BACKGROUND:The role of the alternative complement pathway and its mediation by retinal microglia and macrophages, is well-established in the pathogenesis of Age-Related Macular Degeneration (AMD). However, the contribution of the classical complement pathway towards the progression of retinal degenerations is not fully understood, including the role of complement component 1q (C1q) as a critical activator molecule of the classical pathway. Here, we investigated the contribution of C1q to progressive photoreceptor loss and neuroinflammation in retinal degenerations. METHODS:Wild-type (WT), C1qa knockout (C1qa-/-) and mice treated with a C1q inhibitor (ANX-M1; Annexon Biosciences), were exposed to photo-oxidative damage (PD) and were observed for progressive lesion development. Retinal function was assessed by electroretinography, followed by histological analyses to assess photoreceptor degeneration. Retinal inflammation was investigated through complement activation, macrophage recruitment and inflammasome expression using western blotting, qPCR and immunofluorescence. C1q was localised in human AMD donor retinas using immunohistochemistry. RESULTS:PD mice had increased levels of C1qa which correlated with increasing photoreceptor cell death and macrophage recruitment. C1qa-/- mice did not show any differences in photoreceptor loss or inflammation at 7 days compared to WT, however at 14 days after the onset of damage, C1qa-/- retinas displayed less photoreceptor cell death, reduced microglia/macrophage recruitment to the photoreceptor lesion, and higher visual function. C1qa-/- mice displayed reduced inflammasome and IL-1? expression in microglia and macrophages in the degenerating retina. Retinal neutralisation of C1q, using an intravitreally-delivered anti-C1q antibody, reduced the progression of retinal degeneration following PD, while systemic delivery had no effect. Finally, retinal C1q was found to be expressed by subretinal microglia/macrophages located in the outer retina of early AMD donor eyes, and in mouse PD retinas. CONCLUSIONS:Our data implicate subretinal macrophages, C1q and the classical pathway in progressive retinal degeneration. We demonstrate a role of local C1q produced by microglia/macrophages as an instigator of inflammasome activation and inflammation. Crucially, we have shown that retinal C1q neutralisation during disease progression may slow retinal atrophy, providing a novel strategy for the treatment of complement-mediated retinal degenerations including AMD.

Dataset Information

Transcriptome data and gene ontology analysis in human macrophages ingesting modified lipoproteins in the presence or absence of complement protein C1q.

Publications

Transcriptome data and gene ontology analysis in human macrophages ingesting modified lipoproteins in the presence or absence of complement protein C1q.

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