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Cellular milieu of the neural retina informs complement immune regulation

ABSTRACT: Cellular milieu of the neural retina informs complement immune regulation

PROVIDER: PRJNA483791 | ENA |

REPOSITORIES: ENA

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

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

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

Project description: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

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Cellular milieu of the neural retina informs complement immune regulation

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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.

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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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