溶血磷脂酰胆碱酰基转移酶3调控内皮细胞激活

Llyso-PL Acyltransferases 3 Regulates Endothelial Cell Activation

目的探究溶血磷脂酰胆碱酰基转移酶3(Lyso-PL Acyltransferases 3,LPCAT3)在湍流(Oscillatory Flow,OSS)介导的内皮细胞激活中的作用。方法于2020年11月—2023年6月济宁市第一人民医院分离5只C57BL/6雄性小鼠的主动脉弓(AorticArch,AA)及胸主动脉(ThoracicAorta,TA),用于提取mRNA检测LPCAT3的表达。将原代内皮细胞随机分为对照组(Static)和研究组(OSS),检测LPCAT3的mRNA水平。同时,敲减LPCAT3,验证血管细胞黏附因子-1(Vascular Cell Adhesion Molecule 1,VCAM-1)、细胞间黏附因子-1(Intercellular Adhesion Molecule 1,ICAM-1)的mRNA表达。结果与胸主动脉(1±0.42)相比,小鼠主动脉弓LPCAT3的mRNA相对表达水平(2.03±0.5)明显上调,差异有统计学意义(P<0.05)。与研究组mRNA的相对表达水平(2.72±0.72)(3.04±0.56)相比,OSS+siLPCAT3组其VCAM-1及ICAM-1表达明显降低为(1.31±0.4)(1.81±0.51),差异有统计学意义(P均<0.05),这意味着抑制内皮细胞LPCAT3能够明显减少湍流介导的炎症因子的表达。结论LPCAT3能够调控湍流介导的内皮细胞激活。

Objective To explore the role of lyso-PL acyltransferases 3(LPCAT3)in oscillatory flow(OSS)mediated endothelial cell activation.Methods Aortic arch(AA)and thoracic aorta(TA)of 5 C57BL/6 male mice were isolated from Jining First People's Hospital from November 2020 to June 2023 for mRNA extraction and detection of LPCAT3 expression.The primary endothelial cells were randomly divided into control group(Static)and study group(OSS)to detect the mRNA level of LPCAT3.At the same time,LPCAT3 was knocked down to verify the mRNA expression of vascular cell adhesion molecule 1(VCAM-1)and intercellular adhesion molecule 1(ICAM-1).Results Compared with thoracic aorta(1±0.42),the mRNA relative expression level of LPCAT3 in mouse aortic arch was significantly upregulated(2.03±0.5),and the difference was statistically significant(P<0.05).The mRNA expression level of LPCAT3 in endothelial cells of the study group was 1.88 times higher than that of the control group,and the difference was sta⁃tistically significant(P<0.05).Compared with the mRNA relative expression level of the study group(2.72±0.72)(3.04±0.56),the expression of VCAM-1 and ICAM-1 in OSS+siLPCAT3 group was significantly decreased (1.31±0.4)(1.81±0.51),and the differences were statistically significant(both P<0.05).This implied that inhibition of endothelial LPCAT3 can significantly reduce the expression of turbulence-mediated inflammatory factors.Conclusion LPCAT3 regulates turbulence-mediated endothelial cell activation.