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Dysregulated mesenchymal PDGFR-β drives kidney fibrosis

ABSTRACT: Dysregulated mesenchymal PDGFR-β drives kidney fibrosis

PROVIDER: PRJNA577448 | ENA |

REPOSITORIES: ENA

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Dysregulated mesenchymal PDGFR-β drives kidney fibrosis

Project description:Kidney fibrosis is characterized by expansion and activation of platelet-derived growth factor receptor-β (PDGFR-β) positive mesenchymal cells. To study the consequences of PDGFR-ß activation, we developed a model of primary renal fibrosis using transgenic mice with PDGFR-β activation specifically in renal mesenchymal cells, driving their pathological proliferation and phenotypic switch towards myofibroblasts. This resulted in progressive mesangioproliferative glomerulonephritis, mesangial sclerosis and interstitial fibrosis with progressive anemia due to loss of erythropoietin production by fibroblasts. We used microarrays to compare wildtype animals (Foxd1_wt Pdgfrb_wt) to animals with constitutive mesenchymal PDGFR-β activation (Foxd1_mt Pdgfrb V536A) in the kidney to identify target genes of PDGFR-β signaling.

2019-12-06 | GSE138819 | GEO

Dysregulated mesenchymal PDGFR-? drives kidney fibrosis

Project description: Not available

| S-SCDT-EMM-2019-11021 | biostudies-other

Dysregulated mesenchymal PDGFR-? drives kidney fibrosis.

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| S-EPMC7059015 | biostudies-literature

Synectin Promotes Fibrogenesis by Regulating PDGFR Isoforms Through Distinct Mechanisms

Project description:The scaffold protein synectin plays a critical role in the trafficking and regulation of membrane receptor pathways. As the platelet derived growth factor receptor (PDGFR) pathway is essential for hepatic stellate cell (HSC) activation and liver fibrosis, we sought to determine the role of synectin on the PDGFR pathway in HSC. To study the role of synectin in the development of liver fibrosis, mice with selective deletion of synectin from HSC were generated and found to be protected from fibrosis. RNAseq revealed that knockdown of synectin in HSC demonstrated reductions in the fibrosis pathway of genes including PDGFR-β, but not PDGFR-α. Chromatin Immunoprecipitation assay of the PDGFR-β promoter upon synectin knockdown revealed a pattern of histone marks associated with decreased transcription, dependent on p300. In contradistinction, synectin was found to regulate PDGFR-α through an alternative mechanism: protection from autophagic degradation. Site directed mutagenesis revealed that ubiquitination of specific PDGFR-α lysine residues is responsible for its autophagic degradation. Furthermore, functional studies showed decreased PDGF dependent proliferation and migration after synectin knockdown. Finally, human cirrhotic livers demonstrated increased synectin expression. This work provides insight into differential transcriptional and post-translational mechanisms of synectin regulation of PDGFRs, which are critical to fibrogenesis.

2017-12-31 | GSE93629 | GEO

Novel epigenetically dysregulated genes in Oral Submucous Fibrosis

Project description:Novel epigenetically dysregulated genes in Oral Submucous Fibrosis

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PDGFR-? and kidney fibrosis.

Project description: Not available

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SARS-CoV-2 infects the human kidney and drives fibrosis in kidney organoids

Project description:SARS-CoV-2 infects the human kidney and drives fibrosis in kidney organoids

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Microarray profiling identifies extracellular circulating miRNAs dysregulated in cystic fibrosis

Project description:Microarray profiling identifies extracellular circulating miRNAs dysregulated in cystic fibrosis

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Dysregulated TLR7 signaling drives anemia via development of unique hemophagocyte

Project description:Dysregulated TLR7 signaling drives anemia via development of unique hemophagocyte

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Consequences of beta-PDGFR deletion on hepatic stellate cells during hepatic regeneration

Project description:Purpose: The goal of this study was to determine biological consequences during liver regeneration following partial hepatectomy in mice by next-generation sequencing. A particular interest was to compare mice with either a floxed b-PDGFR allele to mice that harbored a deletion of b-PDGFR in hepatic stellate cells (HSCs), by crossing b-PDGFR fl/fl mice with transgenic GFAP-Cre mice. Methods: b-PDGFR fl/fl mice or mice with a HSC-specific deletion of b-PDGFR underwent either sham operation or 70% partial hepatectomy. Following 72 hours, livers were collected and total RNA was extracted using tizol, followed by a purification using Quiagen spin columns including an on-column DNAse digestion step. Conclusion: Our study represents a detailed analysis of hepatic transcriptome, with biologic replicates, generated by RNA-seq technology of livers following sham operation or partial hepatectomy in b-PDGFR fl/fl mice or b-PDGFRfl/fl/GRAP-Cre mice.

2013-11-08 | GSE52234 | GEO

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