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MicroRNA expression data from human corneal epithelial cells exposed to media, human tear, media + P. aeruginosa antigens, tear + P. aeruginosa antigens

ABSTRACT: Exposure to tear fluid can enhance corneal epithelial cells' ability to resist bacterial virulence mechanisms by upregulating epithelial-derived innate defense genes. The aim of this study was to further elucidate the mechanisms by which tear fluid modulates epithelial cell susceptibility to P. aeruginosa internalization and the relationship to known to be upregulated genes with tear fluid exposure. The hypothesis tested was that tear fluid effects on epithelial cells involve the induction of microRNA expression to modify innate defense gene responses to bacterial challenge.

ORGANISM(S): synthetic construct Homo sapiens

PROVIDER: GSE39341 | GEO | 2012/07/14

SECONDARY ACCESSION(S): PRJNA170674

REPOSITORIES: GEO

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Project description:Myosteatosis is the pathological accumulation of lipid that occurs in conjunction with atrophy and fibrosis following skeletal muscle injury or disease. Little is known about the mechanisms by which lipid accumulates in myosteatosis, but many studies have demonstrated the degree of lipid infiltration negatively correlates with muscle function and regeneration. Our goal was to identify biochemical pathways that lead to muscle dysfunction and lipid accumulation in injured rotator cuff muscles, a model that demonstrates severe myosteatosis. Adult rats were subjected to a massive tear to the rotator cuff musculature. After a period of either 0 (healthy control), 10, 30, or 60 days, muscles were prepared for RNA sequencing, shotgun lipidomics, metabolomics, biochemical measures, electron microscopy, and muscle fiber contractility. Following rotator cuff injury, there was a decrease in muscle fiber specific force production that was lowest at 30d. There was a dramatic time dependent increase in triacylglyceride content. Interestingly, genes related to not only triacylglyceride synthesis, but also lipid oxidation were largely downregulated over time. Using bioinformatics techniques, we identified that biochemical pathways related to mitochondrial dysfunction and reactive oxygen species were considerably increased in muscles with myosteatosis. Long chain acyl-carnitines and L-carnitine, precursors to beta-oxidation, were depleted following rotator cuff tear. Electron micrographs showed injured muscles displayed large lipid droplets within mitochondria at early time points, and an accumulation of peripheral segment mitochondria at all time points. Several markers of oxidative stress were elevated following rotator cuff tear. The results from this study suggest that the accumulation of lipid in myosteatosis is not a result of canonical lipid synthesis, but occurs due to decreased lipid oxidation in mitochondria. A failure in lipid utilization by mitochondria would ultimately cause an accumulation of lipid even in the absence of increased synthesis. Further study will identify whether this process is required for the onset of myosteatosis.

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MicroRNA expression data from human corneal epithelial cells exposed to media, human tear, media + P. aeruginosa antigens, tear + P. aeruginosa antigens

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