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NEDD4L mediates intestinal epithelial cell ferroptosis to restrict inflammatory bowel diseases and colorectal tumorigenesis

ABSTRACT: NEDD4L mediates intestinal epithelial cell ferroptosis to restrict inflammatory bowel diseases and colorectal tumorigenesis

PROVIDER: PRJNA1189026 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31429578_1.fastq.gz	Fastqsanger.gz
	SRR31429578_2.fastq.gz	Fastqsanger.gz
	SRR31429579_1.fastq.gz	Fastqsanger.gz
	SRR31429579_2.fastq.gz	Fastqsanger.gz
	SRR31429580_1.fastq.gz	Fastqsanger.gz

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NEDD4L mediates intestinal epithelial cell ferroptosis to restrict inflammatory bowel diseases [colonic tissues without isolation]

Project description:NEDD4L mediates intestinal epithelial cell ferroptosis to restrict inflammatory bowel diseases [colonic tissues without isolation]

| PRJNA1190937 | ENA

NEDD4L mediates intestinal epithelial cell ferroptosis to restrict inflammatory bowel diseases and colorectal tumorigenesis

Project description:To explore the underlying mechanisms of NEDD4L in regulating colitis, colonic tissues from DSS-treated Nedd4lf/f VillinCre (IEC KO) mice and Nedd4lf/f (WT) littermates were subjected to RNA-sequencing analysis.

2024-12-08 | GSE282497 | GEO

NEDD4L mediates intestinal epithelial cell ferroptosis to restrict inflammatory bowel diseases [colonic tissues without isolation]

2024-12-08 | GSE282883 | GEO

NEDD4L mediates intestinal epithelial cell ferroptosis to restrict inflammatory bowel diseases and colorectal tumorigenesis

Project description:Various factors play key roles in maintaining intestine homeostasis. Disruption of the balance may lead to intestinal inflammatory diseases (IBDs) and even colorectal cancer (CRC). Loss or gain of function of many key proteins can result in dysregulated intestinal homeostasis. Our research demonstrated that neural precursor cells expressed developmentally down-regulated 4-like protein (NEDD4L or NEDD4-2), a type of HECT family E3 ubiquitin ligase, played an important role in maintaining intestinal homeostasis. NEDD4L expression was significantly inhibited in intestinal epithelial cells (IECs) of patients with Crohn's disease (CD), ulcerative colitis (UC), and CRC. Global knockout of NEDD4L or its deficiency in IECs exacerbated dextran sulfate sodium (DSS)-/2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis and azoxymethane (AOM)/DSS-induced colorectal cancer. Mechanistically, NEDD4L deficiency in IECs inhibited the key ferroptosis regulator glutathione peroxidase 4 (GPX4) expression by reducing the protein expression of solute carrier family 3 member 2 (SLC3A2) without affecting its gene expression, ultimately promoting DSS-induced IEC ferroptosis. Importantly, ferroptosis inhibitors reduced the susceptibility of NEDD4L-deficient mice to colitis and colitis-associated colorectal cancer (CAC). Thus, NEDD4L is an important regulator in IEC ferroptosis, maintaining intestinal homeostasis, making it a potential clinical target for diagnosing and treating IBDs.

2024-10-24 | PXD057173 |

NEDD4L mediates intestinal epithelial cell ferroptosis to restrict inflammatory bowel diseases and colorectal tumorigenesis-2 untreated mice

2024-10-24 | PXD057172 |

NEDD4L mediates intestinal epithelial cell ferroptosis to restrict inflammatory bowel diseases and colorectal tumorigenesis.

Project description:Various factors play key roles in maintaining intestine homeostasis. Disruption of the balance may lead to inflammatory bowel diseases and even colorectal cancer (CRC). Loss or gain of function of many key proteins can result in dysregulated intestinal homeostasis. Our research demonstrated that neural precursor cells expressed developmentally downregulated 4-like protein (NEDD4L, or NEDD4-2), a type of HECT family E3 ubiquitin ligase, played an important role in maintaining intestinal homeostasis. NEDD4L expression was significantly inhibited in intestinal epithelial cells (IECs) of patients with Crohn's disease, ulcerative colitis, and CRC. Global KO of NEDD4L or its deficiency in IECs exacerbated colitis induced by dextran sulfate sodium (DSS) and 2,4,6-trinitrobenzene sulfonic acid (TNBS) and CRC induced by azoxymethane and DSS. Mechanistically, NEDD4L deficiency in IECs inhibited expression of the key ferroptosis regulator glutathione peroxidase 4 (GPX4) by reducing the protein expression of solute carrier family 3 member 2 (SLC3A2) without affecting its gene expression, ultimately promoting DSS-induced IEC ferroptosis. Importantly, ferroptosis inhibitors reduced the susceptibility of NEDD4L-deficient mice to colitis and colitis-associated CRC. Thus, NEDD4L is an important regulator in IEC ferroptosis, maintaining intestinal homeostasis, making it a potential clinical target for diagnosing and treating IBDs.

| S-EPMC11785928 | biostudies-literature

Bio-psychological factors in inflammatory bowel diseases (LIMBO study)

Project description:Bio-psychological factors in inflammatory bowel diseases (LIMBO study)

| PRJEB43193 | ENA

ATAC-Seq of WT and Nedd4L-cKO Muscle stem cells

Project description:Muscle stem cell quiescence is a complex and dynamic state. In this study we examined the role of the Ubiquitin Protease System in muscle stem cell function and quiescence. Using a genetic mouse model where Nedd4L is selectively deleted in myogenic cells, we characterized the effect of the loss of Nedd4L on muscle stem cells. With RNA-Seq we determined that the genetic deletion of Nedd4L resulted in the transition of the muscle stem cells out of deep quiescence and into Galert. Characterized by the upregulation of cell cycle genes and differentiation genes and loss of expression in numerous known quiescence genes. Nedd4L-cKO muscle stem cells are more prone to differentiation and fail to expand properly in vitro.

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Project description:The IBD-Character cohort (Edinburgh, Oslo, Örebro, Linköping, Zaragoza, Maastricht) included patients with inflammatory bowel diseases (IBD: Crohn's disease, ulcerative colitis) recruited at diagnosis and non-IBD controls. Paired-end RNA sequencing was used for whole blood expression profiling. Raw and normalized counts tables are provided.

2022-03-01 | E-MTAB-11349 | biostudies-arrayexpress

Effect of depletion of NEDD4L on gene expression in EC9706 esophageal squamous cell carcinoma cells

Project description:NEDD4L plays a dual role in cancer. In order to verify its role in esophageal squamous cell carcinoma and the impact of NEDD4L deletion on different signaling pathways and gene expression, we used siRNA to transfect EC9706 cells to explore the role of NEDD4L deletion in esophageal squamous cell carcinoma.

2024-11-27 | GSE252141 | GEO

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