Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, People's Republic of China.
The Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, Harbin, Heilongjiang, 150081, People's Republic of China.
Inflammation. 2017 Dec;40(6):2129-2136. doi: 10.1007/s10753-017-0653-y.
The increasing wall stress as is elicited by arterial hypertension promotes their reorganization in the vessel wall which may lead to arterial stiffening and contractile dysfunction. The nuclear factor of activated T cells 5 (NFAT5) pathway plays a role in regulating growth and differentiation in various cell types. We investigated whether the NFAT5 pathway was involved in the regulation of biomechanical stretch-induced human arterial smooth muscle cell (HUASMC) proliferation, inflammation, and migration. Herein, we showed that stretch promoted the expression of NFAT5 in human arterial smooth muscle cells and regulated through activation of c-Jun N-terminal kinase under these conditions. This may contribute to an improved activity of HUASMCs and thus promote reorganization in vascular remodeling processes such as hypertension-induced arterial stiffening and contractile dysfunction.
动脉高血压引起的壁应力增加促进了血管壁的重新组织，这可能导致动脉僵硬和收缩功能障碍。激活的 T 细胞核因子 5（NFAT5）途径在各种细胞类型的生长和分化调节中发挥作用。我们研究了 NFAT5 途径是否参与调节生物力学拉伸诱导的人动脉平滑肌细胞（HUASMC）增殖、炎症和迁移。在此，我们表明拉伸促进了 NFAT5 在人动脉平滑肌细胞中的表达，并在这些条件下通过激活 c-Jun N 末端激酶进行调节。这可能有助于提高 HUASMC 的活性，从而促进血管重塑过程中的重新组织，如高血压引起的动脉僵硬和收缩功能障碍。
