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Pinch loss in early mesenchymal progenitors alters bone marrow environment

ABSTRACT: Pinch loss in early mesenchymal progenitors alters bone marrow environment

PROVIDER: PRJNA638652 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11990513.fastq.gz	Fastqsanger.gz
	SRR11990514.fastq.gz	Fastqsanger.gz
	SRR11990515.fastq.gz	Fastqsanger.gz
	SRR11990516.fastq.gz	Fastqsanger.gz
	SRR11990517.fastq.gz	Fastqsanger.gz

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Pinch loss in early mesenchymal progenitors alters bone marrow environment

Project description:To investigate the alteration of bone marrow environment caused by Pinch loss, we performed single-cell RNA-sequencing on bone marrow cells, including hematopoietic cells and non-hematopietic stromal cells. As results indicated, we found both cell type proportion and transcriptomic signatures were dramatically altered by Pinch loss. We identified genes related to ossification, extracellular matrix organization, skeletal system development, and vasculature structure development were significantly differentially expressed between control group and dKO group in many mesenchymal stromal cells. Our results revealed Pinch loss disrupted homeostasis of bone marrow niche, monocytes in bone marrow were actively involved in inflammatory response, and functions of mesenchymal stromal cells was severely disrupted.

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Project description:Bone marrow stromal cells (BMSCs) were isolated from the femora and tibiae of irtTA-GBD*-TAg transgenic mice. Using cellular cloning we established skeletal progenitors with unipotent osteogenic and adipogenic properties. Previous RNA-seq analysis of more progenitor types revealed differential expression in members of the Interferon-gamma (IFNγ) signaling pathway. Treatment of adipogenic progenitors with IFNγ inhibited adipogenesis and promoted osteogenesis. RNA-seq analysis of osteogenic, adipogenic and IFNγ treated adipogenic clones revealed factors controlling the osteogenic versus adipogenic commitment of bone marrow skeletal progenitors.

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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.

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