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

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

PROVIDER: PRJNA950458 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24030145_1.fastq.gz	Fastqsanger.gz
	SRR24030145_2.fastq.gz	Fastqsanger.gz
	SRR24030146_1.fastq.gz	Fastqsanger.gz
	SRR24030146_2.fastq.gz	Fastqsanger.gz
	SRR24030147_1.fastq.gz	Fastqsanger.gz

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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

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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.

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

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

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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.

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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.

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

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

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 | GSE189681 | GEO

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

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RNA-seq analsis of control or two P-cadherin knockout HCA-7 cell lines

Project description:RNA-seq analsis of control or two P-cadherin knockout HCA-7 cell lines

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

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