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Role of KLF6 in shaping macrophage inflammatory response

ABSTRACT: Role of KLF6 in shaping macrophage inflammatory response

PROVIDER: PRJNA562566 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10042200.fastq.gz	Fastqsanger.gz
	SRR10042201.fastq.gz	Fastqsanger.gz
	SRR10042202.fastq.gz	Fastqsanger.gz
	SRR10042203.fastq.gz	Fastqsanger.gz
	SRR10042204.fastq.gz	Fastqsanger.gz

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Role of KLF6 in shaping macrophage inflammatory response

Project description:Kruppel-like transcription factor 6 (KLF6) is a member of zinc-finger family transcription factors that regulate critical cellular processes including development, differentiation, proliferation, and programmed cell death. Alterations in KLF6 expression or function has been associated with the pathogenesis of numerous human ailments, including inflammatory bowel diseases, cancer, hepatic steatosis, and hepatic fibrosis.

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Macrophage-KLF6 signaling promotes experimental atherogenesis

Project description:Cardiovascular disease accounts for one in every four deaths in the United States and is the single largest cause of mortality around the world. The most common cause of cardiovascular-related deaths are due to development of occlusive atherosclerotic plaques. A hallmark event in the development of atherosclerotic plaque is the accumulation of lipid-laden macrophages in the subendothelial layers of affected blood vessels. Macrophages are key players in all stages of atherogenesis, including plaque initiation, growth, rupture, as well as healing of ruptured plaques. In this context, macrophages are the principal innate immune cells that modulate atherogenesis by engaging in various processes such as inflammation, extracellular matrix degradation, phagocytosis, and efferocytosis. Here, we report that macrophage Kruppel-like factor 6 (KLF6) deficiency attenuates pro-inflammatory gene expression and experimentally induced atherosclerotic plaque development. Our in vivo studies show that myeloid-KLF6 deficiency on Apoe-null background significantly curtails high-fat/high-cholesterol diet-induced atherosclerotic lesion formation and macrophage abundance in atherosclerotic plaques. Integrated transcriptomics and Gene Set Enrichment Analysis show that KLF6 deficiency significantly attenuates a large number of TNF-induced gene targets, and TNF-induced IFN response, IFN response, and inflammatory response signaling in macrophages. At the molecular level, KLF6 promotes IRF1 signaling to enhance TNF-induced pro-inflammatory gene expression in macrophages. Collectively, our analyses show that KLF6 promotes pro-inflammatory gene expression in macrophages and boosts experimentally induced atherosclerotic plaque formation in vivo.

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