Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of FN14KO on mouse lung immune cells after bleomycin injury

ABSTRACT: TWEAK, also known as TNFSF12, is a multifunctional cytokine that controls many cellular activities in tissue repair and disease by binding to its receptor Fn14.TWEAK-Fn14 signaling has been shown to induce canonical and noncanonical NFkB signaling, triggering pro-inflammatory responses and leukocyte infiltration.In the bleomycin-induced lung fibrosis model, Fn14 KO mice were found to induce a more severe fibrotic phenotype. To explore the effect of Fn14 KO on immune cell populations in this model, we performed single-cell sequencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE262928 | GEO | 2025/01/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	GSE262928_RAW.tar	Raw
	filelist.txt	Txt

Items per page:

1 - 3 of 3

Similar Datasets

Effect of tweak stimulation on primary lung fibroblasts

Project description:TWEAK, also known as TNFSF12, is a multifunctional cytokine that controls many cellular activities in tissue repair and disease by binding to its receptor Fn14.TWEAK-Fn14 signaling has been shown to induce canonical and noncanonical NFkB signaling, triggering pro-inflammatory responses and leukocyte infiltration.We found that TWEAK-Fn14 signaling was upregulated in IPF while Fn14 was mainly expressed in fibroblasts. Therefore, we added different concentrations of TWEAK to primary mouse lung fibroblasts to activate the TWEAK-Fn14 signaling pathway, and explored the transcriptome changes of TWEAK-Fn14 signaling pathway activation in fibroblasts by RNA-seq technology.

2025-01-20 | GSE262923 | GEO

Ionizing radiation in GI tract of Tweak KO mice

2011-07-01 | GSE25029 | GEO

Ionizing radiation in GI tract of Tweak KO mice

Project description:TWEAK/Fn14 signaling may regulate the expression of genes involved in epithelial repair and mucosal inflammation. Comparing the gene signatures in WT and TWEAK KO mice will inform the biology of TWEAK/Fn14 pathway in the GI tract. Mice were treated with 3 Gy of ionizing radiation. After 6h and 24h mice were sacrificed, and whole colon and jejunum were harvested, and RNA was isolated from these tissues. Each CEL file represents a different mouse.

2011-07-01 | E-GEOD-25029 | biostudies-arrayexpress

TMT-coupled phosphoproteomics support novel role of TWEAK/Fn14 signaling in synaptic function

Project description:The study aims at illustrate novel role of TWEAK/Fn14 signaling in synapse function by combining electrophysiological and phosphoproteomic approaches. The results show that TWEAK acutely dampens basal synaptic transmission and plasticity through neuronal Fn14 and impacts the phosphorylation state of pre- and post-synaptic proteins in adult mouse hippocampal slices. Two models featuring synaptic deficits were used in the study. Blocking TWEAK/Fn14 signaling augments synaptic function in hippocampal slices from amyloid beta-overexpressing mice. After stroke, genetic or pharmacological inhibition of TWEAK/Fn14 signaling augments basal synaptic transmission and normalizes plasticity. Our data support a glial/neuronal axis that critically modifies synaptic physiology and pathophysiology in different contexts in the mature brain and may be a therapeutic target for improving neurophysiological outcomes.

2021-02-02 | PXD021582 | Pride

Chronic TNBS Colitis in the FN14 KO Mouse

Project description:To test TWEAK/Fn14 pathway and relative agents in chronic TNBS colitis Chronic colitis was induced by rectal injection of TNBS with ethanol for 6 weeks in WT or FN14 KO BALB/c mice. Colons were harvested for gene profiling.

2013-06-20 | E-GEOD-36806 | biostudies-arrayexpress

The cytokine receptor Fn14 regulates neuronal transcription during development and brain function in the adult [ATAC-seq]

Project description:Signaling between the cytokine TWEAK and its receptor Fn14 is critical for neural circuit development in the postnatal brain. However, the downstream mechanisms through which TWEAK and Fn14 mediate synapse development have remained unclear. Here, we apply single-nucleus RNA-sequencing to Fn14 and TWEAK KO mice to characterize the genes that are regulated by this pathway in the developing dorsal lateral geniculate nucleus of the thalamus at single-cell resolution. We identify robust cohorts of genes that are misregulated in the absence of either Fn14 or TWEAK, providing insight into the transcriptional mechanisms through which cytokine signaling between microglia and neurons regulates a key phase of postnatal brain development that is driven by sensory experience.

2024-10-25 | GSE186631 | GEO

The cytokine receptor Fn14 regulates neuronal transcription during development and brain function in the adult [RNA-seq]

2024-10-25 | GSE186630 | GEO

Th17 cells secrete TWEAK to trigger epithelial-mesenchymal transition and promote colorectal cancer liver metastasis (scRNA-seq)

Project description:Liver metastasis is the leading cause of mortality in patients with colorectal cancer (CRC). Given the significance of both epithelial-mesenchymal transition (EMT) of tumor cells and the immune microenvironment in CRC liver metastasis (CRLM), the interplay between them could hold the key for developing improved treatment options. We employed multi-omics analysis of 130 samples from 18 synchronous CRLM patients integrated with external datasets to comprehensively evaluate the interaction between immune cells and EMT of tumor cells in liver metastasis. Single-cell RNA sequencing analysis revealed distinct distributions of non-malignant cells between primary tumors from patients with metastatic CRC (mCRC) and non-metastatic CRC, showing that Th17 cells were predominantly enriched in the primary lesion of mCRC. TWEAK, a cytokine secreted by Th17 cells, promoted EMT by binding to receptor Fn14 on tumor cells, and the TWEAK-Fn14 interaction enhanced tumor migration and invasion. In mouse models, targeting Fn14 using CRISPR-induced knockout or lipid-nanoparticle-encapsulated siRNA alleviated metastasis and prolonged survival. Mice lacking Il17a or Tnfsf12 (encoding TWEAK) exhibited fewer metastases compared to wild-type mice, while co-transfer of Th17 with tumor cells promoted liver metastasis. Higher TWEAK expression was associated with a worse prognosis in CRC patients. Additionally, CD163L1+ macrophages interacted with Th17 cells, recruiting Th17 via the CCL4-CCR5 axis. Collectively, this study unveils the role of immune cells in the EMT process and identifies TWEAK secreted by Th17 as a driver of CRLM.

2024-01-05 | GSE245552 | GEO

Th17 cells secrete TWEAK to trigger epithelial-mesenchymal transition and promote colorectal cancer liver metastasis (RNA-seq)

2024-02-06 | GSE255163 | GEO

Th17 cells secrete TWEAK to trigger epithelial-mesenchymal transition and promote colorectal cancer liver metastasis (WES)

2024-02-06 | GSE255165 | GEO