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Recombinant Human Soluble Thrombomodulin Suppresses Monocyte Adhesion by Reducing Lipopolysaccharide-Induced Endothelial Cellular Stiffening.
Cells ( IF 6 ) Pub Date : 2020-07-30 , DOI: 10.3390/cells9081811
Takayuki Okamoto 1 , Eiji Kawamoto 2, 3 , Haruki Usuda 1 , Tetsuya Tanaka 1, 4 , Tetsuro Nikai 5 , Kunihiro Asanuma 6 , Koji Suzuki 7 , Motomu Shimaoka 2 , Koichiro Wada 1
Affiliation  

Endothelial cellular stiffening has been observed not only in inflamed cultured endothelial cells but also in the endothelium of atherosclerotic regions, which is an underlying cause of monocyte adhesion and accumulation. Although recombinant soluble thrombomodulin (rsTM) has been reported to suppress the inflammatory response of endothelial cells, its role in regulating endothelial cellular stiffness remains unclear. The purpose of this study was to investigate the impact of anticoagulant rsTM on lipopolysaccharide (LPS)-induced endothelial cellular stiffening. We show that LPS increases endothelial cellular stiffness by using atomic force microscopy and that rsTM reduces LPS-induced cellular stiffening not only through the attenuation of actin fiber and focal adhesion formation but also via the improvement of gap junction functionality. Moreover, post-administration of rsTM, after LPS stimulation, attenuated LPS-induced cellular stiffening. We also found that endothelial cells regulate leukocyte adhesion in a substrate- and cellular stiffness-dependent manner. Our result show that LPS-induced cellular stiffening enhances monocytic THP-1 cell line adhesion, whereas rsTM suppresses THP-1 cell adhesion to inflamed endothelial cells by reducing cellular stiffness. Endothelial cells increase cellular stiffness in reaction to inflammation, thereby promoting monocyte adhesion. Treatment of rsTM reduced LPS-induced cellular stiffening and suppressed monocyte adhesion in a cellular stiffness-dependent manner.

中文翻译:

重组人可溶性血栓调节素通过减少脂多糖诱导的内皮细胞硬化而抑制单核细胞粘附。

不仅在发炎的培养的内皮细胞中而且在动脉粥样硬化区域的内皮中也观察到内皮细胞的硬化,这是单核细胞粘附和积累的根本原因。尽管据报道重组可溶性血栓调节蛋白(rsTM)抑制内皮细胞的炎症反应,但其在调节内皮细胞僵硬度中的作用仍不清楚。这项研究的目的是研究抗凝rsTM对脂多糖(LPS)诱导的内皮细胞硬化的影响。我们表明,LPS通过使用原子力显微镜提高了内皮细胞的硬度,而rsTM不仅通过肌动蛋白纤维的衰减和粘着斑的形成,而且通过间隙连接功能的改善,降低了LPS诱导的细胞僵硬。此外,LPS刺激后,rsTM给药后减弱了LPS诱导的细胞僵硬。我们还发现内皮细胞以底物和细胞刚度依赖性方式调节白细胞粘附。我们的结果表明,LPS诱导的细胞硬化增强了单核细胞THP-1细胞系的粘附,而rsTM通过降低细胞硬度来抑制THP-1细胞与发炎的内皮细胞的粘附。内皮细胞在对炎症的反应中增加细胞刚度,从而促进单核细胞粘附。rsTM的治疗以依赖于细胞刚度的方式减少了LPS诱导的细胞硬化并抑制了单核细胞粘附。我们还发现内皮细胞以底物和细胞刚度依赖性方式调节白细胞粘附。我们的结果表明,LPS诱导的细胞硬化增强了单核细胞THP-1细胞系的粘附,而rsTM通过降低细胞硬度来抑制THP-1细胞与发炎的内皮细胞的粘附。内皮细胞在对炎症的反应中增加细胞刚度,从而促进单核细胞粘附。rsTM的治疗以依赖于细胞刚度的方式减少了LPS诱导的细胞硬化并抑制了单核细胞粘附。我们还发现,内皮细胞以底物和细胞刚度依赖性方式调节白细胞粘附。我们的结果表明,LPS诱导的细胞硬化增强了单核细胞THP-1细胞系的粘附,而rsTM通过降低细胞硬度来抑制THP-1细胞与发炎的内皮细胞的粘附。内皮细胞在对炎症的反应中增加细胞刚度,从而促进单核细胞粘附。rsTM的治疗以依赖于细胞刚度的方式减少了LPS诱导的细胞硬化并抑制了单核细胞粘附。内皮细胞在对炎症的反应中增加细胞刚度,从而促进单核细胞粘附。rsTM的治疗以依赖于细胞刚度的方式减少了LPS诱导的细胞硬化并抑制了单核细胞粘附。内皮细胞在对炎症的反应中增加细胞刚度,从而促进单核细胞粘附。rsTM的治疗以依赖于细胞刚度的方式减少了LPS诱导的细胞硬化并抑制了单核细胞粘附。
更新日期:2020-07-30
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