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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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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.

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