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首页> 外文期刊>African Journal of Biotechnology >Adenovirus vectors can induce activation of endothelial cells: CD40-CD40L interactions partly participate in the endothelial cells activation induced by adenovirus vectors in an NF-kappaB-dependent manner
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Adenovirus vectors can induce activation of endothelial cells: CD40-CD40L interactions partly participate in the endothelial cells activation induced by adenovirus vectors in an NF-kappaB-dependent manner

机译：腺病毒载体可以诱导内皮细胞活化：CD40-CD40L相互作用以NF-κB依赖性方式部分参与腺病毒载体诱导的内皮细胞活化

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Replication-defective adenovirus vector without both E1 and E3 is one of the most popular tools in transgenic therapies. However, more attention should be paid to adenovirus vectors mediated-gene modified study on endothelial cells (ECs). To verify the possible danger in that process, we explored the effect of adenovirus on ECs in this?study. By using western blot analysis, we showed that the level of both CD40 and CD40L on human umbilical vein endothelial cells (HUVECs) were upregraduated by adenovirus vector infection at 100 multiplicity of infection (MOI). The activation of ECs induced by adenovirus vector infection at MOI 100 can be partly inhibited by a blockade of CD40/CD40L interactions by using the recombinant adenovirus Ad-sCD40LIg or an anti-CD40L monoclonal antibody (mAb)?in vitro. On ECs, blockade of CD40/CD40L decreased the expression of IL (interleukin)-6, IL-8 and intercellular adhesion molecule (ICAM) in adenovirus vector-induced cells. In electrophoretic mobility shift assay (EMSA), both Ad-sCD40LIg and anti-CD40L mAb can attenuate the activity of NF-kappaB (NF-κB) pathway contributing to the activation of ECs, which indicated that CD40-CD40L interactions played significant role in the activation of ECs induced by adenovirus vectors via an NF-κB pathway. Our study provide evidences for a supplementary mechanism of the ECs activation induced by adenovirus vector infection and suggests that CD40-CD40L interactions partly participate in the ECs activation induced by adenovirus vectors in an NF-κB-dependent manner.
机译：同时没有E1和E3的复制缺陷型腺病毒载体是转基因治疗中最受欢迎的工具之一。但是，应更加注意腺病毒载体介导的对内皮细胞（EC）的基因修饰研究。为了验证该过程中可能存在的危险，我们在这项研究中探讨了腺病毒对EC的影响。通过蛋白质印迹分析，我们显示人脐静脉内皮细胞（HUVECs）上CD40和CD40L的水平都被腺病毒载体感染以100感染复数（MOI）升级。通过在体外使用重组腺病毒Ad-sCD40LIg或抗CD40L单克隆抗体（mAb）阻断CD40 / CD40L相互作用，可以部分抑制MOI 100上腺病毒载体感染诱导的EC激活。在EC上，CD40 / CD40L的阻断降低了腺病毒载体诱导的细胞中IL（白介素）-6，IL-8和细胞间粘附分子（ICAM）的表达。在电泳迁移率变动分析（EMSA）中，Ad-sCD40LIg和抗CD40L mAb均可减弱NF-κB（NF-κB）通路的活性，从而促进EC的激活，这表明CD40-CD40L相互作用在腺病毒载体通过NF-κB途径诱导的EC的激活。我们的研究提供了腺病毒载体感染诱导的ECs激活的补充机制的证据，并表明CD40-CD40L相互作用部分参与了NF-κB依赖性腺病毒载体诱导的ECs激活。

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