Abstract
BackgroundIn vivo studies have demonstrated that reasonable exercise training can improve endothelial function. To confirm the key role of wall shear stress induced by exercise on endothelial cells, and to understand how wall shear stress affects the structure and the function of endothelial cells, it is crucial to design and fabricate an in vitro multi-component parallel-plate flow chamber system which can closely replicate exercise-induced wall shear stress waveforms in artery.MethodsThe in vivo wall shear stress waveforms from the common carotid artery of a healthy volunteer in resting and immediately after 30 min acute aerobic cycling exercise were first calculated by measuring the inner diameter and the center-line blood flow velocity with a color Doppler ultrasound. According to the above in vivo wall shear stress waveforms, we designed and fabricated a parallel-plate flow chamber system with appropriate components based on a lumped parameter hemodynamics model. To validate the feasibility of this system, human umbilical vein endothelial cells (HUVECs) line were cultured within the parallel-plate flow chamber under abovementioned two types of wall shear stress waveforms and the intracellular actin microfilaments and nitric oxide (NO) production level were evaluated using fluorescence microscope.ResultsOur results show that the trends of resting and exercise-induced wall shear stress waveforms, especially the maximal, minimal and mean wall shear stress as well as oscillatory shear index, generated by the parallel-plate flow chamber system are similar to those acquired from the common carotid artery. In addition, the cellular experiments demonstrate that the actin microfilaments and the production of NO within cells exposed to the two different wall shear stress waveforms exhibit different dynamic behaviors; there are larger numbers of actin microfilaments and higher level NO in cells exposed in exercise-induced wall shear stress condition than resting wall shear stress condition.ConclusionThe parallel-plate flow chamber system can well reproduce wall shear stress waveforms acquired from the common carotid artery in resting and immediately after exercise states. Furthermore, it can be used for studying the endothelial cells responses under resting and exercise-induced wall shear stress environments in vitro.
Highlights
In vivo studies have demonstrated that reasonable exercise training can improve endothelial function
In contrast to resting condition, the frequency and the amplitude of exercise-induced wall shear stress waveform increases, it is worth noting that the reversing part of the wall shear stress waveform obviously enhances
We showed that the quantity of actin microfilaments increased and mostly of them were long, continuous, and paralleled with the long axis of cells after 6 h exposure to two wall shear stress waveforms, which is consistent with the report of Galbraith et al [3]
Summary
In vivo studies have demonstrated that reasonable exercise training can improve endothelial function. Endothelial cells (ECs) lining the innermost layer of vascular wall are constantly exposed to frictional pulsatile wall shear stress induced by flowing blood in the vasculature. Many in vivo and in vitro studies have demonstrated that ECs are able to recognize different wall shear stress frequencies, amplitudes and patterns through mechanosensors (e.g., receptor tyrosine kinases, G protein-coupled receptor, integrins, and glycocalyx) located in the cell membrane [1], and transduce these signals into intracellular via different signaling pathways to regulate cell structures and functions [1], and affect vascular tone, permeability, and ECs proliferation, apoptosis, as well as the secretion of vasoactive substances [2]. Under steady and pulsatile laminar wall shear stress conditions in vitro, ECs elongate and align parallel to the blood flow direction through cytoskeletal remodeling [3]. The cells in oscillatory wall shear stress conditions are more likely to appear endothelial dysfunction, which is believed to be the initial step of atherosclerosis formation and development [9]
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