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Comparative transcriptomics analysis of monocytes of heathy human subjects before and after a dietary oxalate load

ABSTRACT: Comparative transcriptomics analysis of monocytes of heathy human subjects before and after a dietary oxalate load

PROVIDER: PRJNA633473 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11805700_1.fastq.gz	Fastqsanger.gz
	SRR11805700_2.fastq.gz	Fastqsanger.gz
	SRR11805701_1.fastq.gz	Fastqsanger.gz
	SRR11805701_2.fastq.gz	Fastqsanger.gz
	SRR11805702_1.fastq.gz	Fastqsanger.gz

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Comparative transcriptomics analysis of monocytes of heathy human subjects before and after a dietary oxalate load

Project description:Next gen RNA Seq analysis was performed to study the effect of oxalate load on the transcriptome of monocytes in healthy human subjects. Healthy subjects consumed a fruit and vegetable smoothie containing high amount of oxalate. Blood was collected from them before and 5 hrs after consumption of the smoothie. Monocytes were purified from the blood and RNA Sequencing was performed by Illumina NextSeq 500 platform. Differential gene expression analysis was performed using DESeq2 considering fold change > + 2.0 with a q value of < 0.05. 1197 genes were found to be differentially expressed which were used for pathway and functional analysis using Ingenuity software.

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Project description:Metabolic dysfunction-associated steatohepatitis (MASH) is on the rise, and with limited pharmacological therapy available, identification of new metabolic targets is urgently needed. Oxalate is a terminal metabolite produced from glyoxylate by lactate dehydrogenase (LDHA). The liver-specific alanine-glyoxylate aminotransferase (AGXT) detoxifies glyoxylate, preventing oxalate accumulation. We report that AGXT is suppressed and LDHA is activated in livers from patients and mice with MASH, leading to oxalate overproduction. In turn, oxalate promotes steatosis in hepatocytes by inhibiting peroxisome proliferator activated receptor-alpha (PPARα) transcription and fatty acid β-oxidation (FAO), and induces monocyte chemotaxis via C-C motif chemokine ligand 2. In male mice with diet-induced MASH, blocking oxalate overproduction through hepatocyte-specific AGXT overexpression or pharmacological inhibition of LDHA potently lower steatosis, inflammation, and fibrosis by inducing PPARα-driven FAO, and suppressing monocyte chemotaxis, nuclear factor-kappaB and transforming growth factor-beta targets. These findings highlight hepatic oxalate overproduction as a new target for the treatment of MASH.

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