Expression data from HUVECs infected with influenza A virus PR8 and CA07

Using human umbilical vein endothelial cells (HUVECs) as cell models, the present study aims to explore the differential miRNAs in influenza virus-infected ECs and analyze their target genes involved in EC permeability regulation. As the results showed, permeability increased and F-actin cytoskeleton reorganized after HUVECs infected with influenza A virus (CA07 or PR8) at 30 MOI. most of these miRNAs were down-regulated after flu infection. It has been reported that PKC, Rho/ROCK, HRas/Raf/MEK/ERK, and Ca2+/CaM pathways are activated by flu infection and play important roles in permeability regulation. When grown to 90% confluency, HUVECs were removed from the culture medium and washed twice with PBS. Cells were infected with influenza A virus in serum-free media at a multiplicity of infection (MOI) of 20~40 and harvested at the indicated time points. The non-infected cells were used as normal control.

以人脐静脉内皮细胞（human umbilical vein endothelial cells, HUVECs）作为细胞模型，本研究旨在探究流感病毒感染内皮细胞后差异表达的微小核糖核酸（microRNAs, miRNAs），并分析其参与内皮细胞通透性调控的靶基因。研究结果显示，以30感染复数（multiplicity of infection, MOI）的甲型流感病毒（CA07或PR8）感染HUVECs后，细胞通透性升高，肌动蛋白丝（F-actin）细胞骨架发生重排；多数此类微小核糖核酸在流感病毒感染后呈下调表达。已有研究表明，蛋白激酶C（PKC）、Rho/ROCK、HRas/Raf/MEK/ERK以及Ca2+/CaM通路可被流感病毒感染激活，并在通透性调控中发挥重要作用。当HUVECs生长至90%汇合度时，弃去培养基，用磷酸盐缓冲液（PBS）洗涤细胞两次；随后将细胞置于无血清培养基中，以20~40的感染复数接种甲型流感病毒，并于指定时间点收集细胞。以未感染的细胞作为正常对照。