scholarly journals Wall Shear Stress Regulates the Proliferation and Migration of Vascular Smooth Muscle Cells Depending on a TGF-β1 Manner

2019 ◽  
Author(s):  
Lan Jia ◽  
Fang Wei ◽  
Lihua Wang ◽  
Haiyan Chen ◽  
Haibo Yu ◽  
...  
Keyword(s):  
Shear Stress ◽  
Smooth Muscle ◽  
Parallel Plate ◽  
Flow Chamber ◽  
Chamber System ◽  
Parallel Plate Flow Chamber ◽  
And Migration ◽  
Vsmcs Proliferation ◽  
Tgf Β1 ◽  
Proliferation And Migration

Abstract Background: Venous intimal hyperplasia (VIH) is the main cause of arteriovenous fistula (AVF) dysfunction. Hemodynamic forces have an important role in VIH. The proliferation and migration of vascular smooth muscle cells (VSMCs) play a crucial role in the development of VIH and TGF-β1 just has the biological function of inducing proliferation and migration of VSMCs. We use parallel plate flow chamber system to simulate different shear stress and investigate whether shear stress regulate VSMCs proliferation and migration through TGF-β1 Methods: Shear stress (SS) was simulated with an ECs/VSMCs cocultured parallel plate flow chamber system. The coculture system was established by plating cells on the two sides of polyethylene terephthalate membrane. The EC side was subjected to different shear stress (Low-SS, Normal-SS and Oscillating-SS), whereas the opposite VSMCs side was maintained under static conditions. Computational fluid dynamics were applied to three-dimensional models of ECs/VSMCs cocultured flow chamber system to estimate the velocity and WSS. The expression of TGF-β1 were analyzed by immunofluorescence assay. VSMCs proliferation and migration assay was performed with the BrdU kit and Transwell system. Results: The expression of TGF-β1 was significantly up-regulated following application of Low-SS and Oscillating-SS, and the distribution of TGF-β1 was transferred to the cell membrane, compared with the static group. The migration and proliferation of cocultured VSMCs were significantly up-regulated after Low-SS and Oscillating-SS. Conclusion: Our results suggest that Low-SS and Oscillating-SS exerts atherosclerotic influences on the ECs and VSMCs in a TGF-β1-dependent process. TGF-β1 increases the proliferation and migration of VSMC and is thought to be a pro-atherogenic effect, which can be used as a new therapeutic target for the treatment of AVF dysfunction. The formation and development of VIH in AVF may be a local hyperplasia process by shear stress-TGF-β1 regulation, which provides new insights into the mechanisms of neointimal hyperplasia.

Wall Shear Stress Determination in a Small-Scale Parallel Plate Flow Chamber Using Laser Doppler Velocimetry Under Laminar, Pulsatile and Low-Reynolds Number Turbulent Flows

2018 ◽  
Vol 140 (6) ◽  
Author(s):  
Hamed Avari ◽  
Kem A. Rogers ◽  
Eric Savory
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Laser Doppler Velocimetry ◽  
Parallel Plate ◽  
Flow Chamber ◽  
Laser Doppler ◽  
Small Scale ◽  
Doppler Velocimetry ◽  
Flow Conditions ◽  
Parallel Plate Flow Chamber

The parallel plate flow chamber (PPFC) has gained popularity due to its applications in fields such as biological tissue engineering. However, most of the studies using PPFC refer to theoretical relations for estimating the wall shear stress (WSS) and, hence, the accuracy of such quantifications remains elusive for anything other than steady laminar flow. In the current study, a laser Doppler velocimetry (LDV) method was used to quantify the flow in a PPFC (H = 1.8 mm × W = 17.5 mm, Dh = 3.26 mm, aspect ratio = 9.72) under steady Re = 990, laminar pulsatile (carotid Re0-mean = 282 as well as a non-zero-mean sinusoidal Re0-mean = 45 pulse) and low-Re turbulent Re = 2750 flow conditions. A mini-LDV probe was applied, and the absolute location of the LDV measuring volume with the respect to the wall was determined using a signal monitoring technique with uncertainties being around ±27 μm. The uniformity of the flow across the span of the channel, as well as the WSS assessment for all the flow conditions, was measured with the uncertainties all being less than 16%. At least two points within the viscous sublayer of the low-Re turbulent flow were measured (with the y+ for the first point < 3) and the WSS was determined using two methods with the differences between the two methods being within 5%. This paper for the first time presents the experimental determination of WSS using LDV in a small-scale PPFC under various flow conditions, the challenges associated with each condition, and a comparison between the cases. The present data will be useful for those conducting biological or numerical modeling studies using such devices.

scholarly journals Effects of Caveolin-1-ERK1/2 pathway on endothelial cells and smooth muscle cells under shear stress

2019 ◽  
Vol 245 (1) ◽  
pp. 21-33 ◽  
Author(s):  
Lan Jia ◽  
Lihua Wang ◽  
Fang Wei ◽  
Chen Li ◽  
Zhe Wang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Caveolin 1 ◽  
Low Shear Stress ◽  
And Migration ◽  
Oscillating Shear Stress ◽  
Low Shear ◽  
Proliferation And Migration

Hemodynamic forces have an important role in venous intimal hyperplasia, which is the main cause of arteriovenous fistula dysfunction. Endothelial cells (ECs) constantly exposed to the shear stress of blood flow, converted the mechanical stimuli into intracellular signals, and interacted with the underlying vascular smooth muscle cells (VSMCs). Caveolin-1 is one of the important mechanoreceptors on cytomembrane, which is related to vascular abnormalities. Extracellular signal-regulated kinase1/2 (ERK1/2) pathway is involved in the process of VSMCs proliferation and migration. In the present study, we explore the effects of Caveolin-1-ERK1/2 pathway and uremia toxins on the endothelial cells and VSMCs following shear stress application. Different shear stress was simulated with a ECs/VSMCs cocultured parallel-plate flow chamber system. Low shear stress and oscillating shear stress up-regulated the expression of fibroblast growth factor-4, platelet-derived growth factor-BB, vascular endothelial growth factor-A, ERK1/2 phosphorylation in endothelial cells, and proliferation and migration of VSMCs but down-regulated the Caveolin-1 expression in endothelial cells. Uremia toxin induces the proliferation and migration of VSMCs but not in a Caveolin-1-dependent manner in the static environment. Low shear stress-induced proliferation and migration of VSMCs is inhibited by Caveolin-1 overexpression and ERK1/2 suppression. Shear stress-regulated VSMC proliferation and migration is an endothelial cells-dependent process. Low shear stress and oscillating shear stress exert atherosclerotic influences on endothelial cells and VSMCs. Low shear stress modulated proliferation and migration of VSMCs through Caveolin-1-ERK1/2 pathway, which suggested that Caveolin-1 and ERK1/2 can be used as a new therapeutic target for the treatment of arteriovenous fistula dysfunction. Impact statement Venous intimal hyperplasia is the leading cause of arteriovenous fistula (AVF) dysfunction. This article reports that shear stress-regulated vascular smooth muscle cells (VSMCs) proliferation and migration is an endothelial cell (EC)-dependent process. Low shear stress (LSS) and oscillating shear stress (OSS) exert atherosclerotic influences on the ECs and VSMCs. LSS-induced proliferation and migration of VSMCs is inhibited by Caveolin-1 overexpression and extracellular signal-regulated kinase1/2 (ERK1/2) suppression, which suggested that Caveolin-1 and ERK1/2 can be used as a new therapeutic target for the treatment of AVF dysfunction.

scholarly journals MicroRNA-183-5p acts as a potential diagnostic biomarker for atherosclerosis and regulates the growth of vascular smooth muscle cell

2019 ◽  
Author(s):  
Bin Sun ◽  
Zhengkun Shan ◽  
Guoyu Sun ◽  
Xiaolong Wang
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Roc Analysis ◽  
High Specificity ◽  
Diagnostic Value ◽  
Clinical Value ◽  
Specificity And Sensitivity ◽  
And Migration ◽  
Vsmcs Proliferation ◽  
Proliferation And Migration

Abstract Background Atherosclerosis (AS) is a multifactorial chronic disease, and vascular smooth muscle cells (VSMCs) plays an important role in the pathology of AS. MicroRNAs regulate multiple cellular biological processes. This study aimed to investigate the clinical value of miR-183-5p in AS patients, and further explored the effects of miR-183-5p on the proliferation and migration of VSMCs. Methods qRT-PCR was used to test the level of miR-183-5p. The diagnostic value of miR-183-5p for AS patients was assessed by a receiver operating characteristic (ROC) analysis. Cell proliferation and migration were determined via CCK-8 and Transwell assay. Results MiR-183-5p was highly expressed in AS patients compared with the healthy group. Serum miR-183-5p expression was positively associated with CIMT and CRP in AS patients. The ROC analysis suggested that miR-183-5p had quality to be used as a biomarker with high specificity and sensitivity for AS detection. Overexpression of miR-183-5p promoted the proliferation and migration of VSMCs. Downregulation of miR-183-5p attenuated ox-LDL stimulated VSMCs proliferation and migration. Conclusion MiR-183-5p is highly expressed in AS patients, and downregulation of miR-183-5p attenuated ox-LDL stimulated VSMCs proliferation and migration. MiR-183-5p may be a key molecular for the diagnosis and treatment of AS in the future.

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