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Acetate increases the maturation of the preterm intestinal epithelium

ABSTRACT: Acetate increases the maturation of the preterm intestinal epithelium

PROVIDER: PRJEB64402 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR11729057_1.fastq.gz	Fastqsanger.gz
	ERR11729057_2.fastq.gz	Fastqsanger.gz
	ERR11729058_1.fastq.gz	Fastqsanger.gz
	ERR11729058_2.fastq.gz	Fastqsanger.gz
	ERR11729059_1.fastq.gz	Fastqsanger.gz

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Targeting CFTR and FGF2 and TGFβ1 Pathways with MSC-Derived Extracellular Vesicles to Promote Functional Maturation of Preterm Intestinal Epithelium

Project description:Preterm birth disrupts the critical maturation of the intestinal epithelium, leading to compromised digestive and absorptive functions. This study explores the potential of mesenchymal stem cell (MSC)-derived extracellular vesicles (EVs) to promote the maturation of human preterm intestinal epithelial cells. By establishing human preterm intestinal organoids derived from the ileal tissue of a neonate born at 27 weeks gestational age, we demonstrate that treatment with EVs, particularly the EV39 line, significantly enhances the expression of adult-type enterocyte markers, including genes involved in lipid and nutrient transport, digestive enzymes, and epithelial barrier integrity. These maturation signatures were identified through reanalysis of multiple single-cell RNA sequencing (scRNA-seq) datasets, revealing distinct enterocyte differentiation trajectories and key maturation-specific gene expression profiles. Notably, these maturation effects were dependent on cystic fibrosis transmembrane conductance regulator (CFTR) activity, as CFTR inhibition reversed the observed benefits. Proteomic analysis identified FGF2 and TGFβ1 as key ligands mediating the effects of EV39. Co-treatment with FGF2 and TGFβ1 further enhanced epithelial barrier integrity and fatty acid uptake, highlighting the translational potential of EV39 or its ligands in promoting intestinal functional maturation in preterm infants.

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Preterm birth increases susceptibility to hyperglycemia-induced glomerular alterations in the kidneys of male mice [scRNA-seq]

Project description:Diabetic kidney disease (DKD) is the leading cause of progressive chronic kidney disease in adults in the United States. However, the impact of preterm birth on the progression of DKD has not been studied. The goal of this project is to determine the effect of preterm birth on kidney health in a diabetic mouse model. CD-1 pups born preterm (19 days post conception (dpc)) and term (20 dpc) were studied, and outcomes of the male mice were reported, all compared to term mice. Preterm and term mice were treated with streptozotocin at six weeks to induce hyperglycemia. Body weight and blood sugar were monitored. Histologic, molecular, and imaging techniques were used to characterize the mice at 18 weeks. The preterm mice with diabetes had a lower podocyte density, lower proximal tubular fraction, and more atubular glomeruli compared to the term mice without diabetes. They also had a lower podocyte density and lower renin expression compared to term mice with diabetes. Based on single-cell RNA sequencing, preterm mice with diabetes had increased expression of genes related to the angiogenesis migration pathway-related in endothelial cells and increased expression of genes in the actin adhesion pathway in podocytes compared to term mice with diabetes. Furthermore, the preterm mice with diabetes exhibited a weaker endothelial cell-podocyte interaction compared to term mice with diabetes. These data suggest that preterm birth increases susceptibility to glomerular and tubular damage after a brief “second hit” of hyperglycemia. In conclusion, preterm birth disrupts endothelial-podocyte crosstalk and increases susceptibility to kidney injury induced by hyperglycemia.

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Preterm birth increases endogenous human milk peptide release compared to term birth

Project description:Hundreds of naturally occurring milk peptides have been found in term human milk. Whether there are differences between the levels of these peptides between term and preterm milk remains unknown. Premature milk is produced before complete maturation of the mammary gland and is under the influence of a different hormonal milieu, which could change enzymatic activity and protein expression within the mammary gland and result in an altered peptide profile. We employed nano-liquid chromatography tandem mass spectrometry to identify naturally occurring peptides in term and premature milks at multiple time-points across lactation and compare the abundances of these peptides. We found that preterm milks produced more unique peptide sequences than term milks on average (359 vs. 286). The peptides identified were searched for overlapping sequences with an in-house database of known functional peptides. Specifically, we found that both term and preterm milks contain peptides overlapping with known sequences with antimicrobial, opioid antagonist and immunomodulatory actions. We also compared the enzymes involved in degradation of both milks via bioinformatic analysis. This analysis reveals that plasmin is more active in preterm milk than term milk.

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Preterm birth increases susceptibility to hyperglycemia-induced glomerular alterations in the kidneys of male mice [bulk RNA-seq]

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Targeting CFTR and FGF2 and TGFβ1 Pathways with MSC-Derived Extracellular Vesicles to Promote Functional Maturation of Preterm Intestinal Epithelium

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preterm intestinal permeability

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Distinct maternofetal immune signatures delineate preterm birth onset following urinary tract infection

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Transcriptomic analysis delineates preterm prelabor rupture of membranes from preterm labor in preterm fetal membranes

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2024-03-13 | GSE243831 | GEO

Acetate oxidation

Project description:Acetate oxidation

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