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Elevated expression of histone deacetylase HDAC8 suppresses arginine-proline metabolism in necrotizing enterocolitis

ABSTRACT: Elevated expression of histone deacetylase HDAC8 suppresses arginine-proline metabolism in necrotizing enterocolitis

PROVIDER: PRJNA876828 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21422691_1.fastq.gz	Fastqsanger.gz
	SRR21422691_2.fastq.gz	Fastqsanger.gz
	SRR21422692_1.fastq.gz	Fastqsanger.gz
	SRR21422692_2.fastq.gz	Fastqsanger.gz
	SRR21422693_1.fastq.gz	Fastqsanger.gz

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Elevated expression of histone deacetylase HDAC8 suppresses arginine-proline metabolism in necrotizing enterocolitis [RNA-seq]

Project description:Elevated expression of histone deacetylase HDAC8 suppresses arginine-proline metabolism in necrotizing enterocolitis [RNA-seq]

| PRJNA879694 | ENA

Elevated expression of histone deacetylase HDAC8 suppresses arginine-proline metabolism in necrotizing enterocolitis [PCI34051 study]

Project description:Elevated expression of histone deacetylase HDAC8 suppresses arginine-proline metabolism in necrotizing enterocolitis [PCI34051 study]

| PRJNA879722 | ENA

Elevated expression of histone deacetylase HDAC8 suppresses arginine-proline metabolism in necrotizing enterocolitis [CUT&Tag]

Project description:Elevated expression of histone deacetylase HDAC8 suppresses arginine-proline metabolism in necrotizing enterocolitis [CUT&Tag]

| PRJNA879731 | ENA

Elevated expression of histone deacetylase HDAC8 suppresses arginine-proline metabolism in necrotizing enterocolitis

Project description:To further explore the role of HDAC8 in NEC, we analyzed the signaling pathways that were altered in mice with NEC. We then performed gene expression profiling analysis using data obtained from RNA-seq of intestinal tissues (control group, NEC group).

2023-05-04 | GSE212694 | GEO

Elevated expression of histone deacetylase HDAC8 suppresses arginine-proline metabolism in necrotizing enterocolitis [CUT&Tag]

Project description:To verify that arginine metabolic enzymes are directly regulated by H3K9ac, we established FHs74Int cells and HDAC8-overexpressing FHs74Int cells We then performed gene expression profiling analysis using data obtained from CUT&Tag of 4 different treatment conditions in control or HDAC8 stably overexpressed FHs74Int cells ,which treated with PCI34051 (10 µmol/L for 24 h) or LPS (10 µg/ml for 48 h).

2022-09-16 | GSE213190 | GEO

Elevated expression of histone deacetylase HDAC8 suppresses arginine-proline metabolism in necrotizing enterocolitis [RNA-seq]

Project description:To determine which signaling pathway may have been affected by HDAC8, we designed NEC mice model with PCI34051 supplementation. We then performed gene expression profiling analysis using data obtained from RNA-seq of intestinal tissues (control group, NEC group, PCI34051+NEC group) treated with PCI34051 (10 mg/kg/d).

2022-09-16 | GSE213187 | GEO

Elevated expression of histone deacetylase HDAC8 suppresses arginine-proline metabolism in necrotizing enterocolitis.

Project description:Epigenetic alterations are especially important in necrotizing enterocolitis (NEC). Here, we reported that histone deacetylase 8 (HDAC8) plays a previously unknown role in modulating arginine metabolism via acetylation of histone 3 lysine 9 (acetyl-H3K9) regulation during the pathogenesis of NEC. We found that HDAC8 was upregulated in humans and mice intestinal samples with NEC, while selective inhibition of HDAC8 expression ameliorated NEC. HDAC8 regulates enzymes involved in the metabolic conversion of proline to arginine (PRODH, PRODH2, OAT, and OTC) and arginine to ornithine (ARG1). The results showed that H3K9ac signal in the PRODH/PRODH2 promoter region was mediated by HDAC8. Additionally, the decreased concentration of butyric acid was strongly correlated with elevated HDAC8 levels and circulating arginine, which may result from an unbalanced Firmicutes/Bacteroidetes ratio. These results reveal previously underappreciated roles of microbial metabolites and HDAC8 to coordinate the arginine metabolism during NEC development.

| S-EPMC10227426 | biostudies-literature

Elevated expression of histone deacetylase HDAC8 suppresses arginine-proline metabolism in necrotizing enterocolitis [PCI34051 study]

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-09-16 | GSE213191 | GEO

Microfluidic Device Facilitates In Vitro Modeling of Human Neonatal Necrotizing Enterocolitis-on-a-Chip

Project description:Necrotizing enterocolitis is an intestinal disease induces rapid destruction of the epithelial monolayer of the neonatal intestine. Clinically relevant models of this disease are lacking. Using our novel microfluidic model of necrotizing enterocolitis, we characterized the response of intestinal epithelial cell-derived organoids to intestinal bacteria isolated from a neonate with fatal NEC. We subsequently used RNA-sequencing to determine the gene expression profile of these cells after 24 or 72 hours of incubation.

2023-06-14 | GSE226086 | GEO

Amniotic fluid and necrotizing enterocolitis in preterm pigs

Project description:Preterm neonates are susceptible to gastrointestinal (GI) disorders such as necrotizing enterocolitis (NEC). Maternal milk, and especially colostrum, protects against NEC via growth promoting, immunomodulatory and antimicrobial factors. The fetal enteral diet, amniotic fluid (AF), contains similar bioactive components and we hypothesized that postnatal AF administration would reduce inflammatory responses and NEC in preterm neonates. Thirty preterm pigs (92% gestation) were delivered by caesarean section and fed total parental nutrition (TPN) for 48 h followed by enteral porcine colostrum (COLOS, n=7), infant formula (FORM, n=13) or formula + porcine AF (AF, n=10). Using a previously validated model of NEC in preterm pigs, we determined the structural, functional, microbiological and immunological responses to AF when administered prior to and after introduction of a suboptimal enteral formula diet. Keywords: Healthy versus inflammed tissues in relation to necrotizing enterocolitis

2010-03-01 | GSE13515 | GEO

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