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Pretreatment of aged mice with retinoic acid restores alveolar regeneration via upregulation of reciprocal PDGFRA signaling

ABSTRACT: Pretreatment of aged mice with retinoic acid restores alveolar regeneration via upregulation of reciprocal PDGFRA signaling

PROVIDER: PRJNA661311 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12583049_1.fastq.gz	Fastqsanger.gz
	SRR12583049_2.fastq.gz	Fastqsanger.gz
	SRR12583050_1.fastq.gz	Fastqsanger.gz
	SRR12583050_2.fastq.gz	Fastqsanger.gz
	SRR12583051_1.fastq.gz	Fastqsanger.gz

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Pretreatment of aged mice with retinoic acid restores alveolar regeneration via upregulation of reciprocal PDGFRA signaling

Project description:Reciprocal PDGFA signaling activates regenerative fibroblasts that support alveolar epithelial cell differentiation and repair, providing a potential therapeutic strategy to influence the pathogenesis of IPF.

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miRNA Expression in PDGFRA Mutant GISTs

Project description:Context: Gastrointestinal stromal tumors (GISTs) harboring mutations in the PDGFRA gene occur in only about 5–7% of patients. The most common PDGFRA mutation is exon 18 D842V, which is corre-lated with specific clinico-pathological features compared to the other PDGFRA mutated GISTs. Herein, we present a miRNA expression profile comparison of PDGFRA D842V mutant GISTs and PDGFRA with mutations other than D842V (non-D842V). miRNA expression profiling was carried out on 10 patients using a TLDA miRNA array. Then, miRNA expression was followed by bioinformatic analysis aimed at evaluating differential expression, pathway enrichment, and miRNA-mRNA networks. We highlighted 24 differentially expressed miRNAs between D842V and non-D842V GIST patients. Pathway enrichment analysis showed that deregulated miRNAs targeted genes that are mainly involved in the immune response pathways. The miRNA-mRNA networks highlighted a signature of miRNAs/mRNA that could explain the indolent behavior of the D842V mutated GIST. The results highlighted a different miRNA fingerprint in PDGFRA D842V GISTs compared to non-D842Vmutated patients, which could explain the different bio-logical behavior of this GIST subset.

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Analysis of Nestin-GFP+ pericytes from adipose tissue: PDGFRa wild type versus PDGFRa+/D842V (constitutively active mutant)

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Effects of PDGFRa-lineage leukocyte extravasation to skin in atopic dermatitis

Project description:The circulating leukocyte population contains a fraction of cells derived from progenitors that had transient PDGFRa expression during embryonic development (PDGFRa-lineage). During inflammation, extravasated leukocytes in inflamed tissue modify the tissue-resident leukocyte population and crosstalk with the stromal cells. The current study investigates the effects of extravasated leukocytes derived from PDGFRa-lineage origin on the skin in atopic dermatitis (AD). Lineage- bone marrow progenitors were isolated from PDGFRa-lineage labeling mice which labels cells derived from PDGFRa-lineage with tdTomato. Progenitors derived from PDGFRa-lineage or non-PDGFRa-lineage were transplanted to irradiated EGFP-transgenic mice and allowed for bone marrow reconstitution (BMT). AD was then induced by repeated topical application of MC903 for six times. On day 14, RNA was isolated from inflamed skin to construct library for bulk RNA sequencing. AD skin transcriptomes of PDGFRa-lineage and non-PDGFRa-lineage BMTs were compared. In addition, the obtained dataset were paired with flow cytometric measurement of leukocyte extravasation to compare samples with similar extravasation loads. We found via functional enrichment analyses that extravasated PDGFRa-lineage leukocytes possess intrinsic properties that differ from non-PDGFRa-lineage, coordinate stronger inflammatory responses and modulate the extracellular matrix.

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Cells isolated from diaphragm of mdx mouse: satellite cells vs. PDGFRa+ cells

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The single cell RNA seq of PDGFRa-GFP+ cells in mouse lung

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Seawater pretreatment

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Cerebral gene expression changes in Pdgfc and Pdgfra mutant

Project description:Platelet-derived growth factor-C (PDGF-C) is one of three known ligands for the tyrosine kinase receptor PDGFRÎ±. Analysis of Pdgfc null mice has demonstrated roles for PDGF-C in palate closure and the formation of cerebral ventricles, but redundancy with other PDGFRÎ± ligands might hide additional functions. In search of further developmental roles for PDGF-C, we generated mice that were double mutants for Pdgfc -/- and Pdgfra GFP/+. These mice display a range of severe phenotypes including cerebellar malformation, neuronal over-migration in the cerebral cortex, spina bifida and lung emphysema. We focused our analysis on the central nervous system (CNS), where PDGF-C was identified as a critical factor for the formation of meninges and assembly of the glia limitans basement membrane. Meninges freely dissected and released from P0 cerebrum. RNA was isolated using RNeasy micro kit (Qiagen) and quality checked in a 2100 BioAnalyzer (Agilent Technologies, Santa Clara, CA, USA). Transcription profiling was performed with Gene Chip Mouse Gene 1.0 ST array. We compared Pdgfc-/-; Pdgfra GFP/+ mice, with a control group consisting of all littermates (Pdgfc+/+, Pdgfc+/-, Pdgfc-/-, Pdgfc+/+; Pdgfra GFP/+ and Pdgfc+/-; Pdgfra GFP/+). One litter was used, including 4 mutants and 9 controls

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