Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Core TF Foxc1/2 reinforce differentiation of adult podocyte in glomeruli

ABSTRACT: We identified Fox1 and Foxc2 core transcription factors in kidney glomeruli. To investigate their transcriptional regulatory roles in glomeruli, we performed ChIPseq of Foxc1 and Foxc2 in adult mouse kidney glomeruli. The genome wide distribution of Foxc1/2 binding sites revealed they regulated the differentiation and mature state of adult podocyte to maintain kidney homeostatis.

ORGANISM(S): Mus musculus

PROVIDER: GSE116302 | GEO | 2021/03/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Core TF Foxc1/2 reinforce differentiation of adult podocyte in glomeruli

Project description:Core TF Foxc1/2 reinforce differentiation of adult podocyte in glomeruli

| PRJNA478028 | ENA

Foxc1 and Foxc2 are necessary to maintain glomerular podocytes

Project description:Foxc1 and Foxc2 are highly expressed in adult podocytes. To bypass embryonic lethality of Foxc1 and Foxc2 KO, mice ubiquitously expressing inducible-Cre (ROSA26-CreERT2) were mated with floxed-Foxc1 and floxed-Foxc2 mice. We used microarrays to detail effects of deletions of Foxc1 and Foxc2 on podocyte gene expression profiles in adult podocyte in vivo and in vitro.

2018-07-25 | GSE117571 | GEO

FOXC2 and WT1 regulate transcriptional reprogramming during the podocyte response to injury

Project description:In the context of human disease, the mechanisms whereby transcription factors reprogram gene expression in reparative responses to injury are not well understood. We have studied the mechanisms of transcriptional reprogramming in disease using murine kidney podocytes as a model for tissue injury. Podocytes are a crucial component of glomeruli, the filtration units of each nephron. Podocyte injury is the initial event in many processes that lead to End Stage Kidney Disease. FOXC2 is a transcription factor known to regulate gene expression in podocytes. FOXC2 and WT1 are both required for podocyte differentiation. Using murine models and human kidney organoids, we investigated FOXC2-mediated transcriptional reprogramming during the course of podocyte injury. Correlating FOXC2 and WT1 ChIP-seq analyses demonstrated that they co-bind many genes expressed in podocytes. Reprogramming the transcriptome involved highly dynamic changes in the binding of FOXC2 and WT1 to target genes during a reparative injury response.

2023-11-01 | GSE213174 | GEO

Loss of Foxc1 and Foxc2 function in chondroprogenitor cells disrupts endochondral ossification.

Project description:Endochondral ossification forms and grows the majority of the mammalian skeleton and is tightly controlled through gene regulatory networks. The forkhead box transcription factors Foxc1 and Foxc2 have been demonstrated to regulate aspects of osteoblast function in the formation of the skeleton but their roles in chondrocytes to control endochondral ossification are less clear. We demonstrate that Foxc1 expression is directly regulated by SOX9 activity, one of the earliest transcription factors to specify the chondrocyte lineages. Moreover we demonstrate that elevelated expression of Foxc1 promotes chondrocyte differentiation in mouse embryonic stem cells and loss of Foxc1 function inhibits chondrogenesis in vitro. Using chondrocyte-targeted deletion of Foxc1 and Foxc2 in mice, we reveal a role for these factors in chondrocyte differentiation in vivo. Loss of both Foxc1 and Foxc2 caused a general skeletal dysplasia predominantly affecting the vertebral column. The long bones of the limb were smaller and mineralization was reduced and organization of the growth plate was disrupted. In particular, the stacked columnar organization of the proliferative chondrocyte layer was reduced in size and cell proliferation in growth plate chondrocytes was reduced. Differential gene expression analysis indicated disrupted expression patterns in chondrogenesis and ossification genes throughout the entire process of endochondral ossification in Col2-cre;Foxc1Δ/Δ;Foxc2Δ/Δ embryos. Our results suggest that Foxc1 and Foxc2 are required for correct chondrocyte differentiation and function. Loss of both genes results in disorganization of the growth plate, reduced chondrocyte proliferation and delays in chondrocyte hypertrophy that prevents correct ossification of the endochondral skeleton.

2021-09-08 | GSE165951 | GEO

LSAGE Library Human Renal Glomeruli

2007-06-13 | GSE8114 | GEO

Human iPSC-derived glomeruli provide an advanced model to interrogate podocyte biology and accurately recapitulate podocytopathy

Project description:Podocytes are highly specialised cells within the glomeruli of the kidney that maintain the filtration barrier by forming interdigitating foot processes and slit-diaphragms. Disruption to these features result in proteinuria and glomerulosclerosis. Studies into podocyte biology and disease have previously relied on conditionally immortalised cell lines due to the non- proliferative nature of this cell type. Here we describe an advanced model to study both podocyte and glomerular biology using isolated glomeruli from kidney organoids derived from human pluripotent stem cells.

2018-12-04 | GSE111992 | GEO

FOXC1 and FOXC2 promote endothelial-derived R-spondin 3 and CXCL12 signals in intestinal regeneration after ischemia-reperfusion injury

Project description:Intestinal ischemia induces mucosal damage while simultaneously activating intestinal stem cells (ISCs), which subsequently regenerate the damaged intestinal epithelium. However, whether angiocrine factors secreted from vascular endothelial cells (ECs) - blood and lymphatic ECs (BECs and LECs, respectively) – regulate ISC-mediated regeneration have yet to be elucidated. Here, we identify FOXC1 and FOXC2 as essential regulators of angiocrine signaling in regeneration of the small intestine after ischemia-reperfusion (I/R) injury. EC- and LEC-specific deletions of Foxc1, Foxc2, or both in mice augment I/R-induced intestinal damage by causing defects in vascular regrowth, expression of the chemokine CXCL12 and the Wnt activator R-spondin 3 in BECs and LECs, respectively, and activation of Wnt signaling in ISCs. Treatment with CXCL12 and R-spondin 3 rescues the I/R-induced intestinal damage in EC- and LEC-Foxc mutant mice, respectively. This study provides evidence that FOXC1 and FOXC2 are required for intestinal regeneration by stimulating angiocrine CXCL12 and Wnt signaling.

2021-12-13 | GSE190581 | GEO

LSAGE Library Human Renal Glomeruli

Project description:Glomeruli were isolated from the kidney of a 72 yo male patient. The kidney was surgically removed due to renal cell carcinoma. The glomeruli were isolated from uninvolved renal parenchyma. Histology (H&E) of glomeruli and interstitium was normal. Keywords: Kidney Subcompartment Glomeruli were isolated using the sieving technique in ice-cold PBS, followed by isolation of total RNA with RNeasy kit. RNA was judged intact by agarose gel electrophoresis. SAGE library was custom-synthesized by Genzyme Corportation.

2007-06-12 | E-GEOD-8114 | biostudies-arrayexpress

H3K27ac ChIP-seq from human glomeruli

Project description:In order to understand the kidney compartment specific epigenetic feature of glomeruli, we isolated glomeruli from human kidney biopsy and performed H3K27ac ChIP seq.

2021-03-26 | GSE142593 | GEO

Genome-wide profiling of expression of human glomeruli and tubules

Project description:Glomeruli and tubules are two key components in adult kidney cortex, and are important for kidney function. In order to understand the transcriptional regulation of kidney glomeruli and tubules, we generated genome wide transcription profiles with laser isolated glomeruli and tubules. Human Transcriptome 2.0 GeneChips (HTA2.0) were used to examine global gene expression.

2021-03-26 | GSE116034 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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