Collective influence of substrate chemistry with physiological fluid shear stress on human umbilical vein endothelial cells

In the treatment of cardiovascular diseases, vascular scaffold materials play an extremely important role. The appropriate substrate chemistries and 15 dynes/cm(2) physiological fluid shear stress (FSS) are both required to ensure normal physiological activity of human umbilical vein endothelial cells (HUVECs). The present study reported the collective influence of substrate chemistries and FSS on HUVECs in the sense of its biological functions. The CH3, NH2, and OH functional groups were adopted to offer a variety of substrate chemistries on glass slides by the technology of self-assembled monolayers, whereas FSS was generated by a parallel-plate fluid flow system. Substrate chemistries on its own by no means had noticeable effects on eNOS, ATP, NO, and PGI(2) expressions, while FSS stimuli enhanced their production. While substrate chemistries, as well as FSS, were both exerted, the releases of ATP, NO, and PGI(2) were dependent on substrate chemistries. Study of F-actin organization and focal adhesions (FAs) formation of HUVECs before FSS exposure proves that F-action organization and FAs formation followed similar chemistry-dependence. Hereby proposed a feasible mechanism, that is, the F-actin organization and FAs formation of HUVECs are controlled by substrate chemistries, further advancing the modulation of FSS-triggered responses of HUVECs.

Automated summary

The treatment of cardiovascular diseases relies heavily on vascular scaffold materials to ensure normal physiological activity of endothelial cells. This study investigated the combined effects of substrate chemistries and fluid shear stress on HUVECs, showing that FSS enhances the production of key substances while the release of ATP, NO, and PGI(2) is influenced by both substrate chemistries and FSS. The study also suggests that F-actin organization and focal adhesions of HUVECs are controlled by substrate chemistries, which in turn affects the responses triggered by FSS.