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FAM3A Reshapes Vascular Smooth Muscle Cell Fate Specification in Abdominal Aortic Aneurysm by Regulating KLF4 Ubiquitination

ABSTRACT: FAM3A Reshapes Vascular Smooth Muscle Cell Fate Specification in Abdominal Aortic Aneurysm by Regulating KLF4 Ubiquitination

PROVIDER: PRJNA957768 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24227800_1.fastq.gz	Fastqsanger.gz
	SRR24227800_2.fastq.gz	Fastqsanger.gz
	SRR24227801_1.fastq.gz	Fastqsanger.gz
	SRR24227801_2.fastq.gz	Fastqsanger.gz
	SRR24227802_1.fastq.gz	Fastqsanger.gz

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FAM3A Reshapes Vascular Smooth Muscle Cell Fate Specification in Abdominal Aortic Aneurysm by Regulating KLF4 Ubiquitination

Project description:Vascular smooth muscle cell (VSMC) differentiation reprogramming plays an essential role in abdominal aortic aneurysm (AAA). However, the underlying mechanisms are still indistinct. FAM3A (family with sequence similarity 3, member A) is a newly identified metabolism regulator. We examined FAM3A expression and the downstream pathways affected by FAM3A in AAA, and how FAM3A regulated VSMC differentiation. We found that overexpression or supplement of FAM3A significantly attenuated the progression of AAA, manifested by maintenance of VSMC well-differentiation state and inhibition of VSMC transformation towards macrophage-, chondrocyte-, osteogenic-, mesenchymal-, and fibroblast-like cell subpopulations. Importantly, FAM3A induced a decrease in Krüppel-like factor 4 (KLF4) phosphorylation (Ser254) level, leading to its ubiquitination and a weakened nuclear localization. Our findings identify FAM3A as a novel VSMC fate-shaping regulator in AAA and unveil the underpinning mechanism associated with KLF4 ubiquitination and stability, which could develop new strategies based on FAM3A to restore VSMC homeostasis in AAA.

2023-04-23 | GSE230163 | GEO

FAM3A reshapes VSMC fate specification in abdominal aortic aneurysm by regulating KLF4 ubiquitination.

Project description:Reprogramming of vascular smooth muscle cell (VSMC) differentiation plays an essential role in abdominal aortic aneurysm (AAA). However, the underlying mechanisms are still unclear. We explore the expression of FAM3A, a newly identified metabolic cytokine, and whether and how FAM3A regulates VSMC differentiation in AAA. We discover that FAM3A is decreased in the aortas and plasma in AAA patients and murine models. Overexpression or supplementation of FAM3A significantly attenuate the AAA formation, manifested by maintenance of the well-differentiated VSMC status and inhibition of VSMC transformation toward macrophage-, chondrocyte-, osteogenic-, mesenchymal-, and fibroblast-like cell subpopulations. Importantly, FAM3A induces KLF4 ubiquitination and reduces its phosphorylation and nuclear localization. Here, we report FAM3A as a VSMC fate-shaping regulator in AAA and reveal the underlying mechanism associated with KLF4 ubiquitination and stability, which may lead to the development of strategies based on FAM3A to restore VSMC homeostasis in AAA.

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