Mechanical Property of TiO2 Micro/Nano Surface Based on the Investigation of Residual Stress, Tensile Force and Fluid Flow Shear Stress: For Potential Application of Cardiovascular Devices

2017 ◽  
Vol 49 ◽  
pp. 190-201 ◽  
Author(s):  
Cong Zhen Han ◽  
Jing An Li ◽  
Dan Zou ◽  
Xiao Luo ◽  
Ping Yang ◽  
...  
Keyword(s):  
Residual Stress ◽  
Blood Flow ◽  
Shear Stress ◽  
Surface Energy ◽  
Potential Application ◽  
Drug Loading ◽  
Tube Length ◽  
Flow Shear ◽  
Cardiovascular Devices ◽  
Flow Shear Stress

The micro-patterned TiO2 nanotube has been anticipated for potential application for cardiovascular implanted devices for its excellent drug loading/ release function and biocompatibility. However, its mechanical behavior has rarely been studied as the cardiovascular devices. The tube length is a crucial factor which not only decides the drug loading ability but also influences the devices’ mechanical behavior. Therefore, in this work, the micro-patterned TiO2 nanotubes with different tube length (MNT2, MNT4 and MNT6) were fabricated, and their surface energy, residual stress, tensile tolerability and blood flow shear stress tolerability were determined, respectively. The results showed that the microstructure reduced the surface energy of the nanotubes surfaces, enhanced or reduced surface tensile tolerability when parallel or vertical to the strain orientation, and also increased the nanotubes surfaces residual stress; In addition, both micro/nano and single nano surfaces possessed good blood flow shear stress tolerability. These results indicated that the micro/nano surfaces possesses excellent mechanical properties for surface modification of cardiovascular devices.

scholarly journals I022 Role of heme oxygenase-1 in high blood flow (shear stress)-induced remodeling of rat resistance arteries

2009 ◽  
Vol 102 ◽  
pp. S94
Author(s):  
M.-L. Freidja ◽  
E. Vessieres ◽  
B. Toutain ◽  
L. Loufrani ◽  
S. Faure ◽  
...  
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1 ◽  
Resistance Arteries ◽  
Flow Shear ◽  
Flow Shear Stress

scholarly journals Flow shear stress enhances intracellular Ca2+ signaling in pulmonary artery smooth muscle cells from patients with pulmonary arterial hypertension

2014 ◽  
Vol 307 (4) ◽  
pp. C373-C383 ◽  
Author(s):  
Shanshan Song ◽  
Aya Yamamura ◽  
Hisao Yamamura ◽  
Ramon J. Ayon ◽  
Kimberly A. Smith ◽  
...  
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Smooth Muscle ◽  
Pulmonary Arterial Hypertension ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Flow Shear ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Arterial ◽  
Flow Shear Stress

An increase in cytosolic Ca2+ concentration ([Ca2+]cyt) in pulmonary arterial smooth muscle cells (PASMC) is a major trigger for pulmonary vasoconstriction and an important stimulus for pulmonary arterial medial hypertrophy in patients with idiopathic pulmonary arterial hypertension (IPAH). Vascular smooth muscle cells (SMC) sense the blood flow shear stress through interstitial fluid driven by pressure or direct exposure to blood flow in case of endothelial injury. Mechanical stimulus can increase [Ca2+]cyt. Here we report that flow shear stress raised [Ca2+]cyt in PASMC, while the shear stress-mediated rise in [Ca2+]cyt and the protein expression level of TRPM7 and TRPV4 channels were significantly greater in IPAH-PASMC than in normal PASMC. Blockade of TRPM7 by 2-APB or TRPV4 by Ruthenium red inhibited shear stress-induced rise in [Ca2+]cyt in normal and IPAH-PASMC, while activation of TRPM7 by bradykinin or TRPV4 by 4αPDD induced greater increase in [Ca2+]cyt in IPAH-PASMC than in normal PASMC. The bradykinin-mediated activation of TRPM7 also led to a greater increase in [Mg2+]cyt in IPAH-PASMC than in normal PASMC. Knockdown of TRPM7 and TRPV4 by siRNA significantly attenuated the shear stress-mediated [Ca2+]cyt increases in normal and IPAH-PASMC. In conclusion, upregulated mechanosensitive channels (e.g., TRPM7, TRPV4, TRPC6) contribute to the enhanced [Ca2+]cyt increase induced by shear stress in PASMC from IPAH patients. Blockade of the mechanosensitive cation channels may represent a novel therapeutic approach for relieving elevated [Ca2+]cyt in PASMC and thereby inhibiting sustained pulmonary vasoconstriction and pulmonary vascular remodeling in patients with IPAH.

scholarly journals The Effect of Fluid Flow Shear Stress and Substrate Stiffness on Yes-Associated Protein (YAP) Activity and Osteogenesis in Murine Osteosarcoma Cells

Cancers ◽  
2021 ◽  
Vol 13 (13) ◽  
pp. 3128
Author(s):  
Thomas R. Coughlin ◽  
Ali Sana ◽  
Kevin Voss ◽  
Abhilash Gadi ◽  
Upal Basu-Roy ◽  
...  
Keyword(s):  
Shear Stress ◽  
Fluid Flow ◽  
Bone Cells ◽  
Bone Cancer ◽  
Substrate Stiffness ◽  
Flow Shear ◽  
Fluid Movement ◽  
Flow Shear Stress ◽  
Fluid Flow Shear Stress ◽  
New Treatments

Osteosarcoma (OS) is an aggressive bone cancer originating in the mesenchymal lineage. Prognosis for metastatic disease is poor, with a mortality rate of approximately 40%; OS is an aggressive disease for which new treatments are needed. All bone cells are sensitive to their mechanical/physical surroundings and changes in these surroundings can affect their behavior. However, it is not well understood how OS cells specifically respond to fluid movement, or substrate stiffness—two stimuli of relevance in the tumor microenvironment. We used cells from spontaneous OS tumors in a mouse engineered to have a bone-specific knockout of pRb-1 and p53 in the osteoblast lineage. We silenced Sox2 (which regulates YAP) and tested the effect of fluid flow shear stress (FFSS) and substrate stiffness on YAP expression/activity—which was significantly reduced by loss of Sox2, but that effect was reversed by FFSS but not by substrate stiffness. Osteogenic gene expression was also reduced in the absence of Sox2 but again this was reversed by FFSS and remained largely unaffected by substrate stiffness. Thus we described the effect of two distinct stimuli on the mechanosensory and osteogenic profiles of OS cells. Taken together, these data suggest that modulation of fluid movement through, or stiffness levels within, OS tumors could represent a novel consideration in the development of new treatments to prevent their progression.

Temporal gradient in shear-induced signaling pathway: involvement of MAP kinase, c-fos, and connexin43

2000 ◽  
Vol 278 (5) ◽  
pp. H1598-H1605 ◽  
Author(s):  
Xuping Bao ◽  
Craig B. Clark ◽  
John A. Frangos
Keyword(s):  
Shear Stress ◽  
Mrna Expression ◽  
Signaling Pathway ◽  
Steady Shear ◽  
Flow Shear ◽  
Temporal Gradient ◽  
Step Flow ◽  
Shear Component ◽  
Flow Shear Stress ◽  
Impulse Flow

The effect of a temporal gradient in shear and steady shear on the activity of extracellular signal-regulated protein kinases 1 and 2 (ERK1/ERK2), c- fos, and connexin43 (Cx43) in human endothelial cells was investigated. Three laminar flow profiles (16 dyn/cm2), including impulse flow (shear stress abruptly applied for 3 s), ramp flow (shear stress smoothly transitioned at flow onset), and step flow (shear stress abruptly applied at flow onset) were utilized. Relative to static controls, impulse flow stimulated the phosphorylation of ERK1/ERK2 8.5- to 7.5-fold, respectively at 10 min, as well as the mRNA expression of c- fos 51-fold at 30 min, and Cx43 8-fold at 90 min. These high levels of mRNA expression were sustained for at least 4 h. In contrast, ramp flow was unable to significantly induce gene expression and even inhibited the activation of ERK1/ERK2. Step flow, which contains both a sharp temporal gradient in shear stress and a steady shear component, elicited only moderate and transient responses, indicating the distinct role of these fluid shear stimuli in endothelial signal transduction. The specific inhibitor of mitogen-activated protein kinase kinase PD-98059 inhibited impulse flow-induced c -fos and Cx43 mRNA expression. Thus these findings implicate the involvement of ERK1/ERK2, c -fos, and Cx43 in the signaling pathway induced by the temporal gradient in shear.

Microfluidic models of physiological or pathological flow shear stress for cell biology, disease modeling and drug development

2019 ◽  
Vol 117 ◽  
pp. 186-199 ◽  
Author(s):  
Huaying Chen ◽  
Zhihang Yu ◽  
Siwei Bai ◽  
Huaxiu Lu ◽  
Dong Xu ◽  
...  
Keyword(s):  
Shear Stress ◽  
Drug Development ◽  
Cell Biology ◽  
Disease Modeling ◽  
Flow Shear ◽  
Flow Shear Stress
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