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Identification of ethanolamine as a biomarker and therapeutic potential for diabetic retinopathy in glucose well-controlled diabetic patients

ABSTRACT: Identification of ethanolamine as a biomarker and therapeutic potential for diabetic retinopathy in glucose well-controlled diabetic patients

PROVIDER: PRJNA899563 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22235242_1.fastq.gz	Fastqsanger.gz
	SRR22235242_2.fastq.gz	Fastqsanger.gz
	SRR22235243_1.fastq.gz	Fastqsanger.gz
	SRR22235243_2.fastq.gz	Fastqsanger.gz
	SRR22235244_1.fastq.gz	Fastqsanger.gz

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Identification of ethanolamine as a biomarker and therapeutic potential for diabetic retinopathy in glucose well-controlled diabetic patients

Project description:Diabetic retinopathy (DR) is the leading cause of blindness in the working-age population, and there are no diagnostic biomarkers and intervention methods for DR developed from glucose well-controlled diabetic patients (GW-DR) to date. Here, we established a prospective cohort of 2126 diabetic Chinese adults (DM) including1134 subjects without ocular diseases at baseline. After 2-year follow-up, 42 participants (21 new-onset GW-DR and 21 matched control) with HbA1c persistently less than 7% were enrolled to profile the serum metabolic features of GW-DR through targeted metabolomics. Among different levels of metabolites, the lower level of ethanolamine with an AUC of 0.954 was significantly associated with early-stage GW-DR risk compared to HbA1c with a 0.506 AUC. Moreover, ethanolamine attenuated diabetic retinal inflammation in STZ-induced diabetic rats with inactivating microglia and DAG-PKC pathway remodeling. In conclusion, ethanolamine, as a potential metabolic biomarker for early diagnosis of GW-DR, may provide a biomarker-based treatment for DR prevention. We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 different cells at two time points.

2022-11-13 | GSE217573 | GEO

Incipient diabetic retinopathy - Early regulation of genes

Project description:The development of diabetic retinopathy is well characterized on a histological level. Early vascular alterations involve the loss of pericytes. Earlier mechanisms leading to the phenotype of diabetic retinopathy, which involves the complete neurovascular unit, are not yet fully understood. The gene expression data presented here is derived from microarrays and gives further insights into early genetic regulation in incipient diabetic retinopathy.

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Mendelian randomization identifies FLCN expression as a mediator of diabetic retinopathy

Project description:The goal of the study was to identify genes whose aberrant expression can contribute to diabetic retinopathy. We determined differential response in gene expression to high glucose in lymphoblastoid cell lines derived from matched type 1 diabetic individuals with and without retinopathy. Those genes exhibiting the largest difference in glucose response between diabetic subjects with and without retinopathy were assessed for association to diabetic retinopathy utilizing genotype data from a meta-genome-wide association study. All genetic variants associated with gene expression (expression QTLs; eQTLs) of the glucose response genes were tested for association with diabetic retinopathy. We detected an enrichment of the glucose response gene eQTLs among small association p-values for diabetic retinopathy. Among these, we identified FLCN as a susceptibility gene for diabetic retinopathy. Expression of FLCN in response to glucose is greater in individuals with diabetic retinopathy compared to diabetic individuals without retinopathy. Three large, independent cohorts of diabetic individuals revealed an enhanced association of FLCN eQTL to diabetic retinopathy. Mendelian randomization confirmed a direct positive effect of increased FLCN expression on retinopathy in diabetic individuals. Together, our studies integrating genetic association and gene expression implicate FLCN as a disease gene in diabetic retinopathy.

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