Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

FOXF1 inhibits pulmonary fibrosis by preventing CDH2-CDH11 cadherin switch in myofibroblasts

ABSTRACT: FOXF1 inhibits pulmonary fibrosis by preventing CDH2-CDH11 cadherin switch in myofibroblasts

PROVIDER: PRJNA433652 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6703546.fastq.gz	Fastqsanger.gz
	SRR6703547.fastq.gz	Fastqsanger.gz

Items per page:

1 - 2 of 2

Similar Datasets

FOXF1 inhibits pulmonary fibrosis by preventing CDH2-CDH11 cadherin switch in myofibroblasts

Project description:Idiopathic pulmonary fibrosis (IPF) is characterized by aberrant accumulation of collagen-secreting myofibroblasts. Development of effective therapies is limited due to incomplete understanding of molecular mechanisms regulating myofibroblast expansion. FOXF1 transcription factor is expressed in resident lung fibroblasts, but its role in lung fibrosis remains unknown due to the lack of genetic mouse models. Through comprehensive analysis of human IPF genomics data, lung biopsies and transgenic mice with fibroblast-specific inactivation of FOXF1, the present study shows that FOXF1 inhibits pulmonary fibrosis. FOXF1 deletion increases myofibroblast invasion, collagen secretion, and promotes a switch from of N-cadherin (CDH2) to Cadherin-11 (CDH11), which is critical step in acquisition of pro-fibrotic phenotype. FOXF1 directly binds to Cdh2 and Cdh11 promoters and differentially regulates transcription of these genes. Re-expression of CDH2 or inhibition of CDH11 in FOXF1-deficient cells reduces myofibroblast invasion in vitro. FOXF1 inhibits pulmonary fibrosis by regulating a switch from CDH2 to CDH11 in lung myofibroblasts.

2018-08-09 | GSE110408 | GEO

FOXF1 Inhibits Pulmonary Fibrosis by Preventing CDH2-CDH11 Cadherin Switch in Myofibroblasts.

Project description: Not available

| S-EPMC5947867 | biostudies-literature

RNA-seq analsis of siRNA knockdown of cadherin-11 (CDH11) gene in human intestinal myofibroblasts (HIMFs)

Project description:The goal of this experiment was to determine the effect of cadherin-11 (CDH11) knockdown on transcriptional profile of HIMFs

2024-03-01 | GSE228619 | GEO

RNA-seq analsis of siRNA knockdown of cadherin-11 (CDH11) gene in human intestinal myofibroblasts (HIMFs)

Project description:RNA-seq analsis of siRNA knockdown of cadherin-11 (CDH11) gene in human intestinal myofibroblasts (HIMFs)

| PRJNA950458 | ENA

scRNA-seq of fibroblasts from inducible Cdh11 reporter mice

Project description:Cadherin 11 (Cdh11) is a member of the cadherin superfamily, a group of transmembrane proteins that are principally located in adheren junctions and mediate cell-to-cell adhesion. Dysregulation of Cdh11 in fibroblast populations has been associated with pathologic processes such as inflammation, fibrosis, and cancer. We sought to characterise Cdh11+/- lung fibroblast populations using an inducible Cdh11 reporter mouse model.

2026-05-05 | GSE324380 | GEO

Single cell level characterization of Cdh11 deficiency-induced changes in pancreatic cancer

Project description:Cadherin 11 (Cdh11), a cell-to-cell adhesion molecule, has been suggested to promote tumor growth and immunosuppression in PDAC, and Cdh11 inhibition significantly extended survival in mice with PDAC. However, the mechanisms by which Cdh11 deficiency influences PDAC progression and anti-tumor immune responses has yet to be fully elucidated. To investigate Cdh11-deficiency induced changes in PDAC tumor microenvironment (TME), we crossed p48-Cre; LSL-KrasG12D/+; LSL-Trp53R172H/+ (KPC) mice with Cdh11+/- mice and performed single-cell RNA sequencing (scRNA-seq) of the non-immune (CD45-) and immune (CD45+) compartment of KPC tumor bearing Cdh11 proficient (KPC-Cdh11+/+) and Cdh11 deficient (KPC-Cdh11+/-) mice.

2025-05-01 | GSE233915 | GEO

The Forkhead Box F1 Transcription Factor Inhibits Collagen Deposition and Accumulation of Myofibroblasts During Liver Fibrosis

Project description:Hepatic fibrosis is the common end stage to a variety of chronic liver injuries and is characterized by an excessive deposition of extracellular matrix (ECM), which disrupts the liver architecture and impairs liver function. The fibrous lesions are produced by myofibroblasts, which differentiate from hepatic stellate cells (HSC). The myofibroblasts transcriptional networks remain poorly characterized. Previous studies have shown that the Forkhead box F1 (FOXF1) transcription factor is expressed in HSCs and stimulates their activation during acute liver injury; however, the role of FOXF1 in the progression of hepatic fibrosis is unknown. In the present study, we generated αSMACreER;Foxf1fl/fl mice to conditionally inactivate Foxf1 in myofibroblasts during carbon tetrachloride-mediated liver fibrosis. Foxf1 deletion increased collagen depositions and disrupted liver architecture. Timp2 expression was significantly increased in Foxf1-deficient mice while MMP9 activity was reduced. RNA sequencing of purified liver myofibroblasts demonstrated that FOXF1 inhibits expression of pro-fibrotic genes, Col1α2, Col5α2, and Mmp2 in fibrotic livers and binds to active repressors located in promotors and introns of these genes. Overexpression of FOXF1 inhibits Col1a2, Col5a2, and MMP2 in primary murine HSCs in vitro. Altogether, FOXF1 prevents aberrant ECM depositions during hepatic fibrosis by repressing pro-fibrotic gene transcription in myofibroblasts and HSCs.

2019-02-05 | GSE123726 | GEO

The role of cadherin-11 in Unx/AngII induced kidney injury [Huffstater_AA]

Project description:The objective of this study was to understand the impact of losing cadherin-11 (CDH11) on kidney injury. CDH11 has previously been demonstrated to be associated with a number of fibrotic diseases, but its role in kidney injury remains unknown. In vivo models of kidney injury demonstrated improved renal function and reduced tubulointerstitial fibrosis with CDH11 inhibition. However, the mechanism by which CDH11 inhibition mitigates kidney injury is unknown. RNAseq analysis showed altered expression of over 50 genes in two models of kidney injury when CDH11-/- mice were compared with CDH11+/+ mice. These results together indicate that CDH11 deletion alters many genes and pathways that could contribute to kidney injury, including alpha-1 antitrypsin, which is increased in CDH11-/- mice and has been shown to be beneficial in kidney injury.

2024-11-26 | GSE189680 | GEO

The role of cadherin-11 in Unx/AngII induced kidney injury [Huffstater_Unx]

2024-11-26 | GSE189681 | GEO

Loss of cadherin-11 in atherosclerosis immune response: altered macrophage migration and T cell activation

Project description:The objective of this study was to understand the impact of losing cadherin-11 (CDH11) on the immune response in atherosclerosis. CDH11 has previously been demonstrated to be associated with a number of fibrotic diseases, but its exact role in inflammation remains relatively unknown. In vivo models of atherosclerosis demonstrated altered immune cell profiles with CDH11-deficiency, including decreased circulating myeloid cell populations. In vitro studies of CDH11-deficient macrophages revealed increased expression of genes associated with migration, despite a functional decrease in migration, possibly due to compensatory mechanisms. RNAseq analysis also showed increased expression of MHC class II molecule genes in CDH11-/- macrophages, indicating that loss of CDH11 in macrophages could alter T cell populations through increased activation of CD4+ helper T cells. These results together indicate that CDH11 can alter the immune response, in part by impairing macrophage migration and by affecting T cell activation.

2021-09-26 | GSE165942 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data