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

Abstract

In the treatment of cardiovascular diseases, vascular scaffold materials play an extremely important role. The appropriate substrate chemistries and 15 dynes/cm2 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 PGI2 expressions, while FSS stimuli enhanced their production. While substrate chemistries, as well as FSS, were both exerted, the releases of ATP, NO, and PGI2 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.

Development of in vitro microfluidic models to study endothelial responses to pulsatility with different mechanical circulatory support devices

“…Hemodynamic signals, including wall shear stress (WSS) and blood pressure (BP), which vary with cyclic flow characteristics and intensities, have different effects on EC function. For example, hemodynamic signals in the normal physiological range can activate Ca 2+ channels and signaling pathways on EC membranes, causing a dynamic response to the intracellular Ca 2+ concentration [22][23][24][25][26] and promoting the formation of vasodilators, including nitric oxide (NO) in ECs, [27][28][29] thus inhibiting vascular wall inflammation and preventing thrombosis. [27][28][29][30][31][32] However, under the stimulation of some hemodynamic signals in abnormal physiological conditions, the permeability of arterial ECs can be enhanced, and the secretion of pro-inflammatory cytokines, such as reactive oxygen species (ROS) in ECs can increase, [33][34][35][36][37][38] leading to arterial EC dysfunction, which often manifests as local arterial stenosis and ischemia of downstream organs and tissues in the target arteries.…”

“…For example, hemodynamic signals in the normal physiological range can activate Ca 2+ channels and signaling pathways on EC membranes, causing a dynamic response to the intracellular Ca 2+ concentration [22][23][24][25][26] and promoting the formation of vasodilators, including nitric oxide (NO) in ECs, [27][28][29] thus inhibiting vascular wall inflammation and preventing thrombosis. [27][28][29][30][31][32] However, under the stimulation of some hemodynamic signals in abnormal physiological conditions, the permeability of arterial ECs can be enhanced, and the secretion of pro-inflammatory cytokines, such as reactive oxygen species (ROS) in ECs can increase, [33][34][35][36][37][38] leading to arterial EC dysfunction, which often manifests as local arterial stenosis and ischemia of downstream organs and tissues in the target arteries. As treatments for HF, CFVAD and CPD have different effects on the amplitude and frequency of pulsatile hemodynamic signals in arteries, causing abnormal arterial BP and WSS to differentially affect endothelial function.…”