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PDGFRA Defines the Mesenchymal Stem Cell Kaposi’s Sarcoma Progenitors by Enabling KSHV Oncogenesis in an Angiogenic Environment

ABSTRACT: PDGFRA Defines the Mesenchymal Stem Cell Kaposi’s Sarcoma Progenitors by Enabling KSHV Oncogenesis in an Angiogenic Environment

PROVIDER: PRJNA594984 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10673800.fastq.gz	Fastqsanger.gz
	SRR10673800_1.fastq.gz	Fastqsanger.gz
	SRR10673800_2.fastq.gz	Fastqsanger.gz
	SRR10673801.fastq.gz	Fastqsanger.gz
	SRR10673801_1.fastq.gz	Fastqsanger.gz

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PDGFRA Defines the Mesenchymal Stem Cell Kaposi’s Sarcoma Progenitors by Enabling KSHV Oncogenesis in an Angiogenic Environment [ChIP-seq]

Project description:Kaposi’s sarcoma (KS) is an AIDS-defining cancer caused by the KS-associated herpesvirus (KSHV). Unanswered questions regarding KS are its cellular ontology and the conditions conducive to viral oncogenesis. We identify PDGFRA(+)/SCA-1(+) bone marrow-derived mesenchymal stem cells (Pα(+)S MSCs) as KS spindle-cell progenitors and found that pro-angiogenic environmental conditions typical of KS are critical for KSHV sarcomagenesis. This is because growth in KS-like conditions generates a de-repressed KSHV epigenome allowing oncogenic KSHV gene expression in infected Pα(+)S MSCs. Furthermore, these growth conditions allow KSHV-infected Pα(+)S MSCs to overcome KSHV-driven oncogene-induced senescence and cell cycle arrest via a PDGFRA-signaling mechanism; thus identifying PDGFRA not only as a phenotypic determinant for KS-progenitors but also as a critical enabler for viral oncogenesis.

2019-12-12 | GSE141844 | GEO

PDGFRA Defines the Mesenchymal Stem Cell Kaposi’s Sarcoma Progenitors by Enabling KSHV Oncogenesis in an Angiogenic Environment [RNA-seq]

2019-12-12 | GSE141866 | GEO

PDGFRA Defines the Mesenchymal Stem Cell Kaposi’s Sarcoma Progenitors by Enabling KSHV Oncogenesis in an Angiogenic Environment [ChIP-seq]

Project description:PDGFRA Defines the Mesenchymal Stem Cell Kaposi’s Sarcoma Progenitors by Enabling KSHV Oncogenesis in an Angiogenic Environment [ChIP-seq]

| PRJNA594954 | ENA

PDGFRA Defines the Mesenchymal Stem Cell Kaposi’s Sarcoma Progenitors by Enabling KSHV Oncogenesis in an Angiogenic Environment [RNA-seq]

Project description:PDGFRA Defines the Mesenchymal Stem Cell Kaposi’s Sarcoma Progenitors by Enabling KSHV Oncogenesis in an Angiogenic Environment [RNA-seq]

| PRJNA594986 | ENA

PDGFRA Defines the Mesenchymal Stem Cell Kaposi’s Sarcoma Progenitors by Enabling KSHV Oncogenesis in an Angiogenic Environment

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-12-12 | GSE141868 | GEO

PDGFRA defines the mesenchymal stem cell Kaposi's sarcoma progenitors by enabling KSHV oncogenesis in an angiogenic environment.

Project description:Kaposi's sarcoma (KS) is an AIDS-defining cancer caused by the KS-associated herpesvirus (KSHV). Unanswered questions regarding KS are its cellular ontology and the conditions conducive to viral oncogenesis. We identify PDGFRA(+)/SCA-1(+) bone marrow-derived mesenchymal stem cells (Pα(+)S MSCs) as KS spindle-cell progenitors and found that pro-angiogenic environmental conditions typical of KS are critical for KSHV sarcomagenesis. This is because growth in KS-like conditions generates a de-repressed KSHV epigenome allowing oncogenic KSHV gene expression in infected Pα(+)S MSCs. Furthermore, these growth conditions allow KSHV-infected Pα(+)S MSCs to overcome KSHV-driven oncogene-induced senescence and cell cycle arrest via a PDGFRA-signaling mechanism; thus identifying PDGFRA not only as a phenotypic determinant for KS-progenitors but also as a critical enabler for viral oncogenesis.

| S-EPMC6980685 | biostudies-literature

Histone H3.3G34-mutant interneuron progenitors co-opt PDGFRA for gliomagenesis

Project description:Histone H3.3 glycine 34 to arginine/valine (H3.3G34R/V) mutations occur in deadly hemispheric high-grade gliomas. These tumors show exquisite regional and temporal specificity, suggesting a developmental context permissive to the effects of G34R/V mutations. Here we present the molecular landscape of G34R/V gliomas (n = 83) and show that ~50% bear activating mutations in PDGFRA, with strong selection pressure for PDGFRAMUT clones at recurrence. We show that G34R/V tumors arise in interneuron progenitors of the foetal ventral forebrain, expressing GSX2 and the DLX family of homeobox transcription factors, where terminal neuronal differentiation is impaired through aberrant G34R/V-mediated H3K27me3. Frequent co-occurrence of G34R/V & PDGFRAMUT is facilitated in this interneuron lineage-of-origin as PDGFRA forms an aberrant chromatin loop with the adjacent GSX2, hijacking its active chromatin conformation. At the single-cell level, G34R/V tumors entirely lack oligodendroglial transcriptional programs prominent in other glioma entities, and instead harbour dual neuronal and astroglial compartments. CRISPR-removal of H3.3G34R/V does not impact tumorigenicity suggesting this mutation becomes dispensable, while PDGFRAMUT are potently oncogenic regardless of G34 mutation. Collectively, our results suggest that G34R/V gliomas arise in foetal interneuron progenitors unable to terminally differentiate, enabling co-option of PDGFRA through inappropriate expression and activating mutations to promote gliogenesis and oncogenicity. Reliance on PDGFRA for oncogenesis may be of therapeutic opportunity in G34R/V glioma.

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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.

2022-10-31 | GSE215402 | GEO

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

Project description:Analysis of Nestin-GFP+ pericytes flow sorted from 3-day-old mouse cutaneous adipose tissue, comparing controls with wild type PDGFRa, and mutants with increased PDGFRa signaling driven by a Cre/lox-inducible D842V knockin mutation in the PDGFRa kinase domain. The control cells have adipogenic properties in vitro or when transplanted subcutaneously into recipient mice. The D842V mutant cells show altered behavior in the same assays, with poor adipogenic differentiation but a propensity to transition into profibrotic cells that secrete collagen

2015-06-01 | GSE64510 | GEO

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.

2022-07-27 | GSE166854 | GEO

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