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Myeloid specific ASXL2 deletion limits diet induced obesity by regulating energy expenditure

ABSTRACT: Myeloid specific ASXL2 deletion limits diet induced obesity by regulating energy expenditure

PROVIDER: PRJNA602939 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10959600.fastq.gz	Fastqsanger.gz
	SRR10959601.fastq.gz	Fastqsanger.gz
	SRR10959602.fastq.gz	Fastqsanger.gz
	SRR10959603.fastq.gz	Fastqsanger.gz
	SRR10959604.fastq.gz	Fastqsanger.gz

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Myeloid specific ASXL2 deletion limits diet induced obesity by regulating energy expenditure

Project description:We previously reported that global deletion of the Enhancer of Trithorax and Polycomb (ETP) gene, Asxl2, attenuates osteoclast differentiation and also completely protects mice from HFD-induced weight gain. To determine role of this gene specifically in myeloid compartment, ASXL2flox mice were bred with LysM cre (Asxl2LysM). Bone marrow-derived macrophages (BMM) were cultured for 2 days with or without Rank-ligand (RANKL). We characterized the transcriptomic profiles of BMMs and osteoclast by performing unbiased RNA-sequencing. The expression profiles of both macrophages and osteoclast was significantly distinct between two genotypes. In particular, Enrichr analysis of differentially expressed genes (DEG) reveals substantial downregulation of those associated with extracellular matrix (ECM) organization, collagen formation, cytokine-cytokine interaction and inflammatory response including genes encoding TNFα, MMPs and CXCLs, in Asxl2LysM BMMs. In contrast, cell cycle and mitosis related genes are upregulated. The fact that most of the dominant downregulated genes are also implicated in modulating adipose tissue inflammation and fibrosis, supports the concept that genetic deletion of ASXL2, in myeloid cells, may modify obesity.

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