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

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

PROVIDER: PRJNA1190937 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31516982_1.fastq.gz	Fastqsanger.gz
	SRR31516982_2.fastq.gz	Fastqsanger.gz
	SRR31516983_1.fastq.gz	Fastqsanger.gz
	SRR31516983_2.fastq.gz	Fastqsanger.gz
	SRR31516984_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: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 | GSE282883 | GEO

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

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

| PRJNA1189026 | ENA

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

2024-12-08 | GSE282497 | 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 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

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.

2024-05-06 | GSE230620 | GEO

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

RNA-seq of Muscle stem cells (WT and Nedd4L-cKO) and Myoblasts (WT)

2024-05-06 | GSE230621 | GEO

Sonographic detection of massive colonic pseudopolyposis in inflammatory bowel diseases.

Project description:PurposeColonic pseudopolyps are a frequent finding in inflammatory bowel disease (IBD). Yet there are no published data describing the characteristics of pseudopolyposis in intestinal ultrasound (IUS). This study aimed at identifying the key features of pseudopolyposis in IUS.MethodsThis case-control study included 12 patients with ulcerative colitis or Crohn's colitis with extensive left colon pseudopolyposis and 18 matched IBD patients without pseudopolyps at colonoscopy. Luminal (diameters, thickening, stratification, margins, and vascularity) and intraluminal (vascular signals at color Doppler), and extraluminal (mesenteric fat) parameters of the left colon were compared. Anonymized still images and videos of these patients were blindly reviewed to estimate the accuracy in detecting this condition.ResultsAmong the IUS parameters assessed, the anteroposterior diameter ≥ 12 mm and the presence of luminal vascular signals were significantly correlated with pseudopolyposis. The detection of both these findings were able to detect extensive pseudopolyposis a sensitivity of 75% (CI 95%: 42.8-94.5%) and a specificity of 100% (CI 95%: 81.5-100%).ConclusionThis is the first study describing the IUS features of pseudopolyposis in IBD. The potential use of IUS to assess pseudopolyposis might have an impact on IUS monitoring and surveillance of IBD patients with condition.

| S-EPMC10908909 | biostudies-literature

SERBP1 deacetylation inhibits ferroptosis to promote KSHV-induced cellular transformation by decaying lipoyltransferase 2 mRNA

Project description:Ferroptosis, a defensive strategy employed by the host to restrict pathogenic infections, has been implicated in the development and therapeutic responses of various types of tumors. However, the role of ferroptosis in KSHV-induced malignant tumors remains elusive. A steadily growing number of non-histone proteins have been identified as acetylation targets, their functions have yet to be revealed. In this study, we obtained a marked disparity in the landscape of acetylation between MM and KSHV-transformed MM (KMM) cells. SERBP1 deacetylation was upregulated in KMM cells and contributed to KSHV-induced cellular transformation by inhibiting ferroptosis. Mechanistically, KSHV-encoded viral interleukin-6 (vIL-6) hijacks SIRT3, a mitochondrial NAD+-dependent deacetylase, to interact with SERBP1 leading to the deacetylation of SERBP1. Deacetylated SERBP1 exhibits reduced binding to Lipt2 mRNA, which promotes Lipt2 mRNA degradation, resulting in ferroptosis inhibition. Our findings unveil a novel role of SERBP1 deacetylation in regulating ferroptosis and KSHV-induced cellular transformation and identify potential new therapeutic targets for KSHV infection and KSHV-induced cancers.

2023-08-22 | GSE241111 | GEO

Mitochondria preconditioning delays aging and associated diseases in C. elegans impacting on key ferroptosis players

Project description:Excessive iron accumulation or deficiency have detrimental consequences across species, leading to a variety of pathologies in humans. In the nematode Caenorhabditis elegans severe iron as well as oxygen deprivation induce developmental arrest. Instead, hypoxia preconditioning protects against severe hypoxia-induced neuromuscular damage and sub-lethal levels of iron depletion extend lifespan in C. elegans. The positive health outcomes of applying hypoxia preconditioning are obvious but have low feasible application. Here, we thus assessed the potential beneficial effects of genetic and chemical interventions acting via mild iron instead of oxygen depletion. We show that limiting iron availability through frataxin silencing or the iron chelator bipyridine, similar to hypoxia preconditioning, protect against hypoxia-, age- and proteotoxicityinduced neuromuscular deficits. Mechanistically, our data suggest that the beneficial effects elicited by frataxin silencing are at least in part mediated by counteracting ferroptosis, a form of non-apoptotic cell death specifically mediated by iron-induced lipid peroxidation. These is achieved by impacting on different key players of the ferroptosis machinery and likely via novel, gpx-independent redox systems. We thus point to ferroptosis inhibition as a novel strategy to promote healthy aging.

2023-04-17 | PXD040724 | Pride

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