Abstract
UFMylation is a novel ubiquitin-like system that deals with complex and fine-tuned cellular activities and is closely related to endoplasmic reticulum stress. Our previous study indicated that UFMylation is activated in vascular remodeling models. However, the role of UFMylation in atherosclerosis (AS) is unclear. In this study, we investigated changes in UFMylation in ApoE knockout (ApoE-KO) mice. We found that UFMylation was significantly activated in ApoE-KO mice fed a high-fat diet for 46 weeks. Consistently we observed that vascular smooth muscle cells (VSMCs) treated with oxidized low-density lipoprotein (oxLDL) showed UFMylation activation in a time-dependent manner. UFM1-overexpressing mice were generated using transgenic (Tg) technique and bred with ApoE-KO mice to generate ApoE-KO/UFM1-Tg mice. We found that the degree of AS did not vary compared with that of the control. Similarly, overexpression of active UFM1 failed to alter oxLDL-induced proliferation of VSMCs. These findings indicate that UFMylation is activated in AS, but overexpression of UFM1 does not alter the development of AS in ApoE-KO mice.
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