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首页> 外文期刊>Journal of Cellular Physiology >MiR-128-1-5p regulates tight junction induced by selenium deficiency via targeting cell adhesion molecule 1 in broilers vein endothelial cells
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MiR-128-1-5p regulates tight junction induced by selenium deficiency via targeting cell adhesion molecule 1 in broilers vein endothelial cells

机译：mir - 128 - 1 - 5 - p调节引起的紧密连接缺硒通过针对细胞粘附分子1肉鸡静脉内皮细胞

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摘要

Vein endothelial cells (VECs)constitute an important barrier for macromolecules and circulating cells from the blood to the tissues, stabilizing the colloid osmotic pressure of the blood, regulating the vascular tone, and rapidly changing the intercellular connection, and maintaining normal physiological function. Tight junction has been discovered as an important structural basis of intercellular connection and may play a key role in intercellular connection injuries or vascular diseases and selenium (Se) deficiency symptoms. Hence, we replicated the Se-deficient broilers modeland detected the specific microRNA in response to Se-deficient vein by using quantitative real time-PCR (qRT-PCR) analysis. Also, we selected miR-128-1-5p based on differential expression in vein tissue and confirmed its target gene cell adhesion molecule 1 (CADM1) by the dual luciferase reporter assay and qRT-PCR in VECs. We made the ectopic miR-128-1-5p expression for the purpose of validating its function on tight junction. The result showed that miR-128-1-5p and CADM1 were involved in the ZO-1-mediated tight junction, increased paracellular permeability, and arrested cell cycle. We presumed that miR-128-1-5p and Se deficiency might trigger tight junction. Interestingly, miR-128-1-5p inhibitor and fasudil in part hinder the destruction of theintercellular structure caused by Se deficiency. The miR-128-1-5p/CADM1/tight junction axis provides a new avenue toward understanding the mechanism of Se deficiency, revealing a novel regulation model of tight junction injury in vascular diseases.
机译：血管内皮细胞(vec)组成重要的大分子和障碍循环细胞从血液到组织,稳定的胶体渗透压血液、调节血管张力和迅速改变细胞间连接,维持正常的生理功能。结已经作为一个重要的发现基础结构和细胞间连接可能扮演一个关键的角色在细胞间连接受伤或血管疾病和硒(Se)缺乏症状。发现Se-deficient肉鸡管理制度特定的microRNA在回应Se-deficient静脉用真实time-PCR定量(存在)的分析。mir - 128 - 1 - 5 - p基于微分表达式静脉组织并确认其目标基因的细胞由双粘附分子1 (CADM1)荧光素酶报告实验和矢量中存在。使异位mir - 128 - 1 - 5 - p的表达式目的验证其功能的紧结。CADM1参与ZO-1-mediated紧结,paracellular渗透率增加,并逮捕了细胞周期。mir - 128 - 1 - 5 - p和Se不足可能会触发紧密连接。抑制剂和fasudil部分阻碍破坏theintercellular结构引起的缺硒。连接轴向提供了一种新的途径理解本身的机制缺陷,揭示小说监管模式的紧结损伤血管疾病。

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