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Kynurenine monooxygenase (KMO) knockout mouse liver transcriptomics

ABSTRACT: Kynurenine monooxygenase (KMO) knockout mouse liver transcriptomics

PROVIDER: PRJEB62865 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR11526186_1.fastq.gz	Fastqsanger.gz
	ERR11526186_2.fastq.gz	Fastqsanger.gz
	ERR11526187_1.fastq.gz	Fastqsanger.gz
	ERR11526187_2.fastq.gz	Fastqsanger.gz
	ERR11526188_1.fastq.gz	Fastqsanger.gz

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Project description:Elevated brain levels of the essential metals manganese (Mn), copper, or iron induce motor disease. However, mechanisms of metal-induced motor disease are unclear and treatments are lacking. Elucidating the mechanisms of Mn-induced motor disease is particularly important because occupational and environmental Mn overexposure is a global public health problem. To address this, here we combined unbiased transcriptomics and metabolomics with functional studies in a mouse model of human environmental Mn exposure. Transcriptomics unexpectedly revealed that Mn exposure up-regulated expression of metabolic pathways in the brain and liver. Notably, genes in the kynurenine pathway of tryptophan metabolism, which produces neuroactive metabolites that impact neurological function, were up-regulated by Mn. Subsequent unbiased metabolomics revealed that Mn treatment altered kynurenine pathway metabolites in the brain and liver. Functional experiments then demonstrated that pharmacological inhibition of the first and rate-limiting step of the kynurenine pathway fully rescued Mn-induced motor deficits. Finally, elevated Mn directly activates hypoxia-inducible factor (HIF) transcription factors, and additional mechanistic assays identified a role for HIF1, but not HIF2, in regulating expression of hepatic kynurenine pathway genes under physiological or Mn exposure conditions, suggesting that Mn-induced HIF1 activation may contribute to the dysregulation of the kynurenine pathway in Mn toxicity. These findings (1) identify the upregulation of the kynurenine pathway by elevated Mn as a fundamental mechanism of Mn-induced motor deficits; (2) provide a pharmacological approach to treat Mn-induced motor disease; and (3) should broadly advance understanding of the general principles underlying neuromotor deficits caused by metal toxicity.

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RNA-sequencing of inguinal white adipose tissue (iWAT) from kynurenine 3-monooxygenase (Kmo) knockout mice and wild-type littermates on chow and high-fat diets.

Project description:RNA-sequencing of inguinal white adipose tissue (iWAT) from kynurenine 3-monooxygenase (Kmo) knockout mice and wild-type littermates on chow and high-fat diets.

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Nutritional effects by beta-carotene in liver in males and females of control wildtype mice versus BCMO knockout mice

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Project description:BackgroundKynurenine 3-monooxygenase converts kynurenine to 3-hydroxykynurenine, and its inhibition shunts the kynurenine pathway-which is implicated as dysfunctional in various psychiatric disorders-toward enhanced synthesis of kynurenic acid, an antagonist of both α7 nicotinic acetylcholine and N-methyl-D-aspartate receptors. Possibly as a result of reduced kynurenine 3-monooxygenase activity, elevated central nervous system levels of kynurenic acid have been found in patients with psychotic disorders, including schizophrenia.MethodsIn the present study, we investigated adaptive-and possibly regulatory-changes in mice with a targeted deletion of Kmo (Kmo-/-) and characterized the kynurenine 3-monooxygenase-deficient mice using six behavioral assays relevant for the study of schizophrenia.ResultsGenome-wide differential gene expression analyses in the cerebral cortex and cerebellum of these mice identified a network of schizophrenia- and psychosis-related genes, with more pronounced alterations in cerebellar tissue. Kynurenic acid levels were also increased in these brain regions in Kmo-/- mice, with significantly higher levels in the cerebellum than in the cerebrum. Kmo-/- mice exhibited impairments in contextual memory and spent less time than did controls interacting with an unfamiliar mouse in a social interaction paradigm. The mutant animals displayed increased anxiety-like behavior in the elevated plus maze and in a light/dark box. After a D-amphetamine challenge (5 mg/kg, intraperitoneal), Kmo-/- mice showed potentiated horizontal activity in the open field paradigm.ConclusionsTaken together, these results demonstrate that the elimination of Kmo in mice is associated with multiple gene and functional alterations that appear to duplicate aspects of the psychopathology of several neuropsychiatric disorders.

| S-EPMC5812460 | biostudies-literature

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