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Cellular milieu of the neural retina informs complement immune regulation [Hs]

ABSTRACT: Purpose: We present a comprehensive map of the human retinal complement expression at a single-cell resolution, spanning 11 cell types. Methods: Retinal mRNA profiles from were generated by scRNA sequencing (10x Genomics) from a healthy human donor immediately within 4 hours of death. The data was normalized using Seurat. Results: Using an optimized data analysis workflow, we found novel patterns of complement expression in the retina Conclusions: Our landmark atlas provides crucial mechanistic insights in complement immunology

ORGANISM(S): Homo sapiens

PROVIDER: GSE117956 | GEO | 2026/02/01

REPOSITORIES: GEO

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Anatomical-spatial dissection of single-cell retinal transcriptomics paves the road for new horizons in complement immunology [Mm]

Project description:Purpose: We present the first comprehensive map of the murine retinal complement expression at a single-cell resolution from ~92,000 retinal cells, spanning 11 cell types. Methods: Retinal mRNA profiles from 10-week-old wild-type (WT) Black 6 mouse eyes were generated by scRNA sequencing. The data was normalized using Seurat. Results: Using an optimized data analysis workflow, we found novel patterns of complement expression in the retina Conclusions: Our landmark atlas provides crucial mechanistic insights in complement immunology

2020-01-24 | GSE116426 | GEO

Cellular milieu of the neural retina informs complement immune regulation [Hs]

Project description:Cellular milieu of the neural retina informs complement immune regulation [Hs]

| PRJNA483793 | ENA

Cellular milieu of the neural retina informs complement immune regulation

Project description:Cellular milieu of the neural retina informs complement immune regulation

| PRJNA483791 | ENA

Cellular milieu of the neural retina informs complement immune regulation

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-01-24 | GSE117959 | GEO

Decreased sialylation in the mouse retina elicits complement-related microglia response and bipolar cell loss

Project description:Sialylation plays an important role in self-recognition, as well as keeping the complement and innate immune systems in check. It is unclear whether the reduced sialylation as seen during aging and in mice heterozygous for the null mutant of UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase (Gne+/-), an essential enzyme for sialic acid biosynthesis, contributes to retinal inflammation and degeneration. We found a reduction of polysialic acid and trisialic acid expression in several retinal layers in Gne+/- mice at 9 months of age, which was associated with a higher microglial expression of the lysosomal marker CD68. Furthermore, the total number of rod retinal bipolar cells was reduced in 12 months old Gne+/- mice, demonstrating loss of these retinal interneurons that are involved in connecting photoreceptors and ganglion cells. Whole-genome transcriptome analysis showed up-regulation of the complement, inflammation, and apoptosis pathways in the retinas of Gne+/- mice. Particularly, increased gene transcript levels of the complement factors C3 and C4 and the pro-inflammatory cytokine Il-1β were observed by semi-quantitative real-time polymerase chain reaction (sqRT-PCR) in 9 months old Gne+/- mice. The Iincreased expression of CD68, as well as the loss of rod bipolar cells, and increased gene transcription of the complement factor C4, were all prevented after crossing Gne+/- mice with complement factor C3-deficient animals. In conclusion, our data show that retinal hyposialylation in middle-aged Gne+/- mice, at 9 and 12 months of age, was associated with complement-related inflammation and lysosomal microglia response, as well as rod bipolar cells loss, which was absent in animals with a genetic deletion of complement factor C3.

2025-09-15 | GSE275072 | GEO

Anatomical-spatial dissection of single-cell retinal transcriptomics paves the road for new horizons in complement immunology [Mm]

Project description:Anatomical-spatial dissection of single-cell retinal transcriptomics paves the road for new horizons in complement immunology [Mm]

| PRJNA478452 | ENA

Transcriptional profiling of the rat retina after optic nerve crush uncovers sustained activation of the complement cascade and Delta-Notch signaling pathways

Project description:Glaucoma is a multifactorial neurodegenerative disease, characterized by degeneration of the neurons known as retinal ganglion cells (RGCs). Although distinct in vivo animal models have been used to investigate the mechanisms of both RGC degeneration and reorganization of the retina, there has been little progress in developing efficient strategies for neuroprotection in glaucoma. In the present study, we used transcriptomic profiles of Lister Hooded rats’ retinas 2 weeks after optic nerve crush (ONC) and applied systems biology approaches to better understand the molecular mechanisms by which ONC induced the remodeling of the retinal tissue. We calculated the relative expression variability scored as a statistical measure of the variability of transcript abundance in our datasets and found higher variability after ONC. Also, gene expression stability was used as a score of transcription control and we found a reduction in the number of very stably expressed genes from 336 to 124. Enrichment analysis showed that Complement cascade and Notch signaling pathway were the main affected pathways after ONC. In order to deepen our studies on these two pathways, we performed coordination analysis of genes within each pathway and with the entire transcriptome. ONC increased the number of synergistically coordinated pairs of genes and increased the number of similar profiles. This study goes beyond the regulation of individual gene expression showing striking changes in the control of expression by Complement cascade and Notch signaling functional pathways important for RGC degeneration and remodeling of the retinal tissue two weeks after ONC.

2019-07-02 | GSE133563 | GEO

Effects of anti-complement component 5 antibody targeting MG4 domain on the normal retina

Project description:This study aims to investigate the effects of anti-complement component 5 antibody targeting MG4 domain on normal retina.

2017-03-07 | GSE95742 | GEO

Molecular Response of Chorioretinal Endothelial Cells to Complement Injury: Implications for Macular Degeneration

Project description:Age-related macular degeneration (AMD) is a common, blinding disease of the elderly in which macular photoreceptor cells, retinal pigment epithelium, and choriocapillaris endothelial cells ultimately degenerate. Recent studies have found that degeneration of the choriocapillaris occurs early in this disease and that this endothelial cell dropout is concomitant with increased deposition of the complement membrane attack complex (MAC) at the choroidal endothelium. However, the impact of MAC injury to choroidal endothelial cells is poorly understood. To model this event in vitro, and to study the downstream consequences of MAC injury, endothelial cells were exposed to complement from human serum, compared to heat inactivated serum which lacks complement components. Cells exposed to complement components in human serum showed increased labeling with antibodies directed against the MAC, time and dose dependent cell death as assessed by lactate dehydrogenase assay, and increased permeability. RNA-Seq analysis following complement injury revealed increased expression of genes associated with angiogenesis including matrix metalloproteases (MMPs) 3 and 9, and VEGF-A. The MAC-induced increase in MMP9 RNA expression was validated using C5 depleted serum compared to C5 reconstitited serum. Increased levels of MMP9 were also determined using Western blot and zymography. These data suggest that, in addition to cell lysis, complement attack on choroidal endothelial cells promotes an angiogenic phenotype in surviving cells. RNA-Seq of RF/6A (cultured choroidal endothelial cells from Rhesus macaque) treated with either 50% heat-inactivated human serum ([CONTROL], n=3) or 50% normal human serum (active complement membrane attack complex [MAC], n=3)

2015-11-04 | E-GEOD-70806 | biostudies-arrayexpress

Complement Factor H deficiency results in decreased neuroretinal expression of Cd59a in aged mice.

Project description:Purpose: The complement system is closely linked to the pathogenesis of age-related macular degeneration (AMD). Several complement genes are expressed in retinal pigment epithelium (RPE), and complement proteins accumulate in drusen. Further, a common variant of complement factor H (CFH) confers increased risk of developing AMD. Because the mechanisms by which changes in the function of CFH influence development of AMD are unclear, we examined ocular complement expression as a consequence of age in control and CFH null mutant mice. Methods: Gene expression in neuroretinas and RPE/choroid from young and aged WT and Cfh-/- C57BL/6J mice was analysed by microarrays. Expression of a wide range of complement genes was compared to expression in splenocytes and in liver tissue by qRT-PCR. Results: An age-associated increased expression of complement, particularly C1q, C3 and Factor B, in the RPE/choroid coincided with increased expression of the negative regulators Cfh and Cd59a in the neuroretina. Young mice deficient in CFH expressed Cd59a similar to WT, but failed to upregulate Cd59a expression with age. Both hepatic and splenic expression of Cd59a increased with age regardless of Cfh genotype. Conclusions: While the connection between CFH deficiency and failure to up-regulate CD59a remains unknown, these results suggest that expression of CD59 is tissue-specific and that neuroretinal regulation depends on CFH. This could contribute to the visual functional deficits and morphological changes in the Cfh-/- mouse retina that occur with age, and further suggests that deficient neuroretinal regulation of complement could represent an early event in AMD. Gene expression in neuroretinas and RPE/choroid from young and aged WT and Cfh-/- mice, 4 biological replicates in each group.

2012-10-02 | E-GEOD-38671 | biostudies-arrayexpress

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