新生内膜
基因敲除
血管平滑肌
生物
下调和上调
细胞生物学
血小板源性生长因子受体
胚胎血管重塑
内皮干细胞
生长因子
癌症研究
内科学
再狭窄
内分泌学
医学
细胞培养
体外
受体
生物化学
平滑肌
基因
支架
遗传学
作者
Ming Su,Zhihong Yue,Hui Wang,Mei Jia,Congxia Bai,Wei Qiu,Jingzhou Chen
标识
DOI:10.1089/dna.2017.4073
摘要
Vascular remodeling is a key process leading to arterial stenosis. Ufmylation, a novel ubiquitin-like modification, was observed to be associated with many biological processes. However, whether ufmylation is involved in the regulation of vascular remodeling remains unclear. Therefore, the present study focused on the role of ufmylation in vascular remodeling. Mouse femoral artery guidewire injury models were used for inducing vascular remodeling. We found that the expression of Ufm1 was upregulated in hyperplastic neointima. By treating vascular smooth muscle cells (VSMCs) with platelet-derived growth factor BB (PDGF-BB) for 3, 6, 12, and 24 h, respectively, we observed that ufmylation was significantly activated in a time-dependent manner. Consistently, the expression levels of Ufc1, Ufl1, and Ufbp1, as key components of the ufmylation system, were all upregulated by PDGF-BB. In contrast, knockdown of Ufm1 expression attenuated PDGF-BB-induced VSMC proliferation. In addition, we observed that ufmylation was activated by lipopolysaccharide (LPS) in endothelial cells, whereas knockdown of Ufm1 was synergized with LPS-induced endothelial cell injury. These findings indicate that ufmylation may participate in regulation of the VSMC phenotypic switch and endothelial cell injury, which may help in the understanding of vascular remodeling.
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