Fedorov D A, Sidorenko S V, Yusipovich A I, Parshina E Y, Tverskoi A M, Abramicheva P A, Maksimov G V, Orlov S N, Lopina O D, Klimanova E A
Faculty of Biology, Lomonosov Moscow State University, Moscow, 1-12 Leninskie Gory, 119234, Russia.
Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, 32 Vavilova Street, 119991, Russia.
Heliyon. 2021 Sep 29;7(9):e08088. doi: 10.1016/j.heliyon.2021.e08088. eCollection 2021 Sep.
High-salt consumption contributes to the development of hypertension and is considered an independent risk factor for vascular remodelling, cardiac hypertrophy and stroke incidence. Alterations in NO production, inflammation and endothelial cell stiffening are considered now as plausible mediators of cardiovascular dysfunction. We studied early responses of endothelial cells (HUVEC) caused by a moderate increase in extracellular sodium concentration. Exposure of HUVEC to elevated sodium within the physiological range up to 24 h is accompanied by changes in monovalent cations fluxes and Na,K-ATPase activation, and, in turn, results in a significant decrease in the content of , and mRNAs. The expression of and genes, as well as the abundance of cytosolic and nuclear NFAT5 protein, remained unchanged. We assessed the mechanical properties of endothelial cells by estimating Young's modulus and equivalent elastic constant using atomic force and interference microscopy, respectively. These parameters were unaffected by elevated-salt exposure for 24 h. The data obtained suggest that even small and short-term elevations of extracellular sodium concentration affect the expression of genes involved in the control of endothelial function through the Na /K -dependent mechanism(s).
高盐摄入会导致高血压的发生，被认为是血管重塑、心脏肥大和中风发生率的独立危险因素。一氧化氮生成、炎症和内皮细胞僵硬的改变现在被认为是心血管功能障碍的可能介质。我们研究了细胞外钠浓度适度增加引起的内皮细胞（人脐静脉内皮细胞）的早期反应。将人脐静脉内皮细胞暴露于生理范围内升高的钠中长达24小时，伴随着单价阳离子通量的变化和钠钾ATP酶的激活，进而导致、和mRNA含量显著降低。和基因的表达以及细胞质和细胞核中NFAT5蛋白的丰度保持不变。我们分别使用原子力显微镜和干涉显微镜通过估计杨氏模量和等效弹性常数来评估内皮细胞的力学性能。这些参数不受24小时高盐暴露的影响。获得的数据表明，即使细胞外钠浓度的小幅短期升高也会通过钠/钾依赖性机制影响参与内皮功能控制的基因表达。
