Molecular Genetic Advances in Uveitis

Hou, Shengping; Kijlstra, Aize; Yang, Peizeng

doi:10.1016/bs.pmbts.2015.04.009

Cited by 35 publications

(26 citation statements)

References 91 publications

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“…This is based upon (genetic) association with numerous immune-related molecules, the frequent occurrence of uveitis in relation to systemic inflammatory conditions, and the beneficial response to immunosuppressive therapy. [8][9][10][11][12] Despite our growing understanding that susceptibility to NIU is in part genetic, and epigenetic modulation contributes to various ocular conditions, studies investigating the epigenetic landscape of uveitis are scarce. [13][14][15] One of the mechanisms through which epigenetic regulation of gene expression takes place is through microRNAs (miRNAs).…”

mentioning

confidence: 99%

A Disease-Associated MicroRNA Cluster Links Inflammatory Pathways and an Altered Composition of Leukocyte Subsets to Noninfectious Uveitis

Verhagen

Bekker

Rossato

et al. 2018

Invest. Ophthalmol. Vis. Sci.

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confidence: 99%

A Disease-Associated MicroRNA Cluster Links Inflammatory Pathways and an Altered Composition of Leukocyte Subsets to Noninfectious Uveitis

Verhagen

Bekker

Rossato

et al. 2018

Invest. Ophthalmol. Vis. Sci.

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“…Currently, it is still unclear for the precise pathogenesis of uveitis. However, an increasing number of evidences indicate that complex genetic backgrounds coupled with aberrant immune responses may be associated with the occurrence and development of uveitis . In the present study, we measured the differentially expressed proteins in EAU rat plasma using an LC‐MS/MS method, performed relevant bioinformatics analyses for these differentially expressed proteins.…”

Section: Discussionmentioning

confidence: 99%

Proteomic Profiling Analysis Reveals a Link between Experimental Autoimmune Uveitis and Complement Activation in Rats

Guo¹,

Tang

et al. 2017

Scand J Immunol

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Uveitis is an autoimmune disease that usually damages the vision function, leading to poor visual quality in patients. As an autoimmune ocular inflammatory disease, the pathogenesis of uveitis is associated with abnormal expression of some proteins and aberrant regulation of multiple signalling pathways. Nevertheless, the detailed mechanism remains unclear. In this study, we induced an experimental autoimmune uveitis (EAU) model in rats. We determined the levels of C3a and membrane attack complex C5b-9 (soluble C5b-9, sC5b-9) in both plasma and aqueous humour, identified the differentially expressed proteins in plasma by liquid chromatography-tandem mass spectrometry and employed bioinformatics algorithms to analyse differentially expressed proteins in EAU rat plasma. The results demonstrate that there were 168 differentially expressed plasma proteins in EAU rats versus control subjects. The levels of sC5b-9 and C3a were elevated in the plasmas and aqueous humours of EAU rats. Gene ontology enrichment analysis showed that the differentially expressed proteins in EAU rat plasma were mainly involved in metabolic and immune processes. Kyoto encyclopedia of genes and genomes (KEGG) pathway annotation, database for annotation, visualization and integrated discovery (DAVID) and protein-protein interaction analyses revealed that the differentially expressed proteins in EAU rat plasmas were closely associated with complement and coagulation cascades, metabolic pathways, NF-kappa B, PI3K-Akt, Toll-like receptors and autophagy. Overall, the differentially expressed proteins in EAU rat plasmas are mainly involved in the complement and coagulation cascades. The pathogenesis of uveitis closely correlates with complement activation.

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“…genomic duplications and deletions, have been increasingly associated with a variety of human genetic disorders, including ocular disorders like hereditary benign epithelial dyskeratosis (HBID) (Allingham et al, 2001; White and Nelson, 1975), AMD (Cantsilieris et al, 2012; Grassmann et al, 2016; Park et al, 2012; Sawitzke et al, 2011; Schmid-Kubista et al, 2009; Sivakumaran et al, 2011), uveitis (Hou et al, 2015) and non-ocular conditions like autism and schizophrenia (Alkan et al, 2011). CNVs are defined as changes in DNA copy number of a specific genomic region when compared to a reference genome.…”

Section: Association Studies In Poagmentioning

confidence: 99%

Major review: Molecular genetics of primary open-angle glaucoma

Liu

Allingham

2017

Experimental Eye Research

123

106

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Glaucoma is a leading cause of irreversible blindness worldwide. Primary open-angle glaucoma (POAG), the most common type, is a complex inherited disorder that is characterized by progressive retinal ganglion cell death, optic nerve head excavation, and visual field loss. The discovery of a large, and growing, number of genetic and chromosomal loci has been shown to contribute to POAG risk, which carry implications for disease pathogenesis. Differential gene expression analyses in glaucoma-affected tissues as well as animal models of POAG are enhancing our mechanistic understanding in this common, blinding disorder. In this review we summarize recent developments in POAG genetics and molecular genetics research.

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Molecular Genetic Advances in Uveitis

Cited by 35 publications

References 91 publications

A Disease-Associated MicroRNA Cluster Links Inflammatory Pathways and an Altered Composition of Leukocyte Subsets to Noninfectious Uveitis

A Disease-Associated MicroRNA Cluster Links Inflammatory Pathways and an Altered Composition of Leukocyte Subsets to Noninfectious Uveitis

Proteomic Profiling Analysis Reveals a Link between Experimental Autoimmune Uveitis and Complement Activation in Rats

Major review: Molecular genetics of primary open-angle glaucoma

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