Department of Cardiology, Shaoxing Second Hospital, Shaoxing, Zhejiang 312000, P.R. China.
Mol Med Rep. 2017 Nov;16(5):6750-6756. doi: 10.3892/mmr.2017.7444. Epub 2017 Sep 8.
The formation of atherosclerosis is recognized to be caused by multiple factors including pathogenesis in monocytes during inflammation. The current study provided evidence that monocytic junctions were significantly altered in patients with atherosclerosis, which suggested an association between cell junctions and atherosclerosis. Claudin‑1, occludin‑1 and ZO‑1 were significantly enhanced in atherosclerosis, indicating that the tight junction pathway was activated during the pathogenesis of atherosclerosis. In addition, the gene expression of 5 connexin members involved in the gap junction pathway were quantified, indicating that connexin 43 and 46 were significantly up‑regulated in atherosclerosis. Furthermore, inflammatory factors including endoglin and SMAD were observed, suggesting that immune regulative factors were down‑regulated in this pathway. Silicon‑based analysis additionally identified that connexins and tight junctions were altered in association with monocytic inflammation regulations, endoglin pathway. The results imply that reduced expression of the immune regulation pathway in monocytes is correlated with the generation of gap junctions and tight junctions which serve important roles in atherosclerosis.
动脉粥样硬化的形成被认为是由多种因素引起的，包括炎症期间单核细胞中的发病机制。本研究提供的证据表明，动脉粥样硬化患者的单核细胞连接明显改变，这表明细胞连接与动脉粥样硬化之间存在关联。Claudin-1、occludin-1 和 ZO-1 在动脉粥样硬化中显著增强，表明紧密连接途径在动脉粥样硬化发病机制中被激活。此外，定量分析了参与缝隙连接途径的 5 个连接子基因的表达，表明缝隙连接蛋白 43 和 46 在动脉粥样硬化中显著上调。此外，观察到包括内皮糖蛋白和 SMAD 在内的炎症因子，表明该途径中的免疫调节因子下调。硅基分析还表明，连接子和紧密连接与单核细胞炎症调节、内皮糖蛋白途径改变相关。结果表明，单核细胞中免疫调节途径的表达降低与缝隙连接和紧密连接的产生相关，而缝隙连接和紧密连接在动脉粥样硬化中起着重要作用。
