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Systems level analysis of lipid metabolism in oxygen-induced retinopathy [liver RNA-Seq]

ABSTRACT: Systems level analysis of lipid metabolism in oxygen-induced retinopathy [liver RNA-Seq]

PROVIDER: PRJNA1186057 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31347574_1.fastq.gz	Fastqsanger.gz
	SRR31347574_2.fastq.gz	Fastqsanger.gz
	SRR31347575_1.fastq.gz	Fastqsanger.gz
	SRR31347575_2.fastq.gz	Fastqsanger.gz
	SRR31347576_1.fastq.gz	Fastqsanger.gz

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Systems level analysis of lipid metabolism in oxygen-induced retinopathy [retina_RNAseq]

Project description:Systems level analysis of lipid metabolism in oxygen-induced retinopathy [retina_RNAseq]

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Systems level analysis of lipid metabolism in oxygen-induced retinopathy [retina_RNAseq]

Project description:Activation of anaplerosis takes away glutamine from the biosynthetic pathway to the energy-producing TCA cycle. Especially, induction of hyperoxia driven anaplerosis in neurovascular tissues such as the retina during early stages of development could deplete biosynthetic precursors from newly proliferating endothelial cells impeding physiological angiogenesis and leading to vasoobliteration. Using an oxygen-induced retinopathy (OIR) mouse model, we investigated the metabolic differences between OIR-resistant BALB/cByJ and OIR susceptible C57BL/6J strains at system levels to understand the molecular underpinnings that potentially contribute to hyperoxia-induced vascular abnormalities in the neural retina. Our systems level in vivo RNA-seq, proteomic, and lipidomic profiling and ex-vivo explant studies show that the medium-chain fatty acids serves as an alternative source to feed the TCA cycle. Our findings strongly implicate that medium-chain fatty acids could suppress glutamine-fueled anaplerosis and ameliorate hyperoxia-induced vascular abnormalities in conditions such as retinopathy of prematurity.

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Urea cycle and 1C/serine metabolism in the prevention of oxygen induced retinopathy

Project description:Untargeted metabolite profiling links the urea cycle and 1C/serine metabolism in the prevention of oxygen induced retinopathy by hepatic HIF stabilization. Premature infants require oxygen supplementation to survive that is simultaneously toxic to developing tissues. We have demonstrated that hypoxia inducible factor (HIF) stabilization during hyperoxia prevents oxygen induced retinopathy (OIR) and lung disease. Here, untargeted metabolite profiling coupled to XCMS systems biology analysis finds that serine/1C and urea cycles dominate pathway enrichment graphs. MS1 peak areas and MS2 library matches reveal 50% or more increased levels of plasma and retina serine, glycine, hypotaurine, methionine, and taurine. In addition, N-acetylglutamate increased 4-fold in serum, while orotate, citrulline, arginine, aspartate, glutamine were at least 50% increased after HIF stabilization. Targeted data analysis in vivo finds that retinal serine and glycine were derived from liver. HIF-1α2lox/2lox; albumin-cre KO had reduced levels of serine and retinal glycine. Inhibition of 1C metabolism blocked rescue by HIF stabilization. The metabolic phenotype of mice protected from OIR by HIF stabilization is dependent on hepatic serine/1C metabolism and urea cycle.

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Project description:Using Next Generation Sequencing (NGS) we profiled miRNA expression in the retina and choroid during degenerative and NV phases of oxygen-induced retinopathy (OIR).

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Project description:High-throughput sequencing of murine retina of the oxygen induced retinopathy (OIR) model compared to control mice at 5 consecutive days (P12-P16)

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