EOLA1通过与MT2A联合抑制ECV304细胞中脂多糖诱导的血管细胞粘附分子-1的表达

IF 2.6 Q3 IMMUNOLOGY
Weiling Leng, Xiaotian Lei, Hao Meng, Xinshou Ouyang, Z. Liang
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引用次数: 6

摘要

本课题组首次在ECV304细胞中发现内皮过表达的脂多糖相关因子1 (EOLA1, GenBank编号AY074889)作为脂多糖(LPS)应答基因。先前的研究进一步证实了EOLA1与金属硫蛋白2A (metallothionein 2A, MT2A)的关联,而EOLA1在lps诱导的ECV304细胞炎症反应中的作用尚不清楚。在本报告中,我们在ECV304细胞中测定了EOLA1的亚细胞定位以及EOLA1对血管细胞粘附分子-1 (VCAM-1)响应LPS的调节能力。我们的研究结果表明,EOLA1在细胞中广泛弥散,并且LPS显著诱导EOLA1的表达。EOLA1敲低导致lps诱导的VCAM-1产生显著增强。与此一致的是,过表达EOLA1导致lps诱导的VCAM-1产生减少。此外,MT2A敲除可减少lps诱导的VCAM-1产生。总之,我们的研究结果表明EOLA1对lps诱导的ECV304细胞中VCAM-1表达的负调控作用涉及其与MT2A的关联。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
EOLA1 Inhibits Lipopolysaccharide-Induced Vascular Cell Adhesion Molecule-1 Expression by Association with MT2A in ECV304 Cells
Our research group firstly discovered endothelial-overexpressed lipopolysaccharide-associated factor 1 (EOLA1, GenBank number AY074889) as a lipopolysaccharide (LPS) responsive gene in ECV304 cells. The previous studies have further demonstrated the association of EOLA1 with metallothionein 2A (MT2A), while the role of EOLA1 during LPS-induced inflammatory response in ECV304 cells is unknown. In this report, we determined the subcellular localization of EOLA1 and the regulatory capacity of EOLA1 on vascular cell adhesion molecule-1 (VCAM-1) in response to LPS in ECV304 cells. Our results show that EOLA1 is broadly diffuse in the cells, and EOLA1 expression is dramatically induced by LPS. EOLA1 knockdown results in significant enhancement of LPS-induced VCAM-1 production. Consistent with this, overexpression of EOLA1 leads to the reduction of LPS-induced VCAM-1 production. Furthermore, MT2A knockdown reduces LPS-induced VCAM-1 production. Collectively, our results demonstrate a negative regulatory role of EOLA1 on LPS-induced VCAM-1 expression involving its association with MT2A in ECV304 cells.
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来源期刊
CiteScore
3.80
自引率
0.00%
发文量
16
审稿时长
16 weeks
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