scholarly journals Physiologically Relevant Fluid-Induced Oscillatory Shear Stress Stimulation of Mesenchymal Stem Cells Enhances the Engineered Valve Matrix Phenotype

2020 ◽  
Vol 7 ◽  
Author(s):  
Brittany A. Gonzalez ◽  
Manuel Perez-Nevarez ◽  
Asad Mirza ◽  
Marcos Gonzalez Perez ◽  
Yih-Mei Lin ◽  
...  
Stem Cells ◽  
2015 ◽  
Vol 33 (2) ◽  
pp. 429-442 ◽  
Author(s):  
Yi-Chun Kuo ◽  
Tzu-Hao Chang ◽  
Wei-Tse Hsu ◽  
Jing Zhou ◽  
Hsiao-Hui Lee ◽  
...  

2011 ◽  
Vol 11 (5) ◽  
pp. 545-556 ◽  
Author(s):  
Huei-Wen Wu ◽  
Chun-Che Lin ◽  
Shiaw-Min Hwang ◽  
Yu-Jen Chang ◽  
Gwo-Bin Lee

2019 ◽  
Vol 234 (9) ◽  
pp. 16312-16319 ◽  
Author(s):  
Danyang Yue ◽  
Mengxue Zhang ◽  
Juan Lu ◽  
Jin Zhou ◽  
Yuying Bai ◽  
...  

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Islam Mohamed ◽  
Sheena Thomas ◽  
Kimberly Rooney ◽  
Roy Sutliff ◽  
Nick Willett ◽  
...  

Introduction: Shear stress forces play an integral role in dictating the endothelial cell (EC) response to changes in blood flow, pro-inflammatory response and hence development of atherosclerosis. Previously, our group has identified EC microRNA-155 (miR-155) as one of the key signature dysregulated miRNAs in areas of chronic low magnitude oscillatory shear stress (OSS) in vasculature and OSS models of in-vitro. Hypothesis: we hypothesized that acute induction of OSS mediates EC oxidative stress, inflammation and dysfunction, via dysregulation of EC miR-155. Methods: 12-week old C57B/6J mice were subjected to abdominal aortic coarctation (AAC), a unique model of acute induction of OSS, for 3 days and downstream segments of acute OSS were compared to upstream unidirectional shear stress (USS) segments of the thoracic aorta. Results: Acute OSS resulted in down regulation of EC miR-155 expression and inverse upregulation of EC RhoA and Myosin light chain kinase (MYLK), known targets of miR-155-mediated EC cytoskeleton organization, in OSS segments compared with USS. This was associated with impaired EC dependent relaxation, differential contractile response to phenylephrine, and loss of EC barrier function as evaluated by extravasation of Evans-blue dye assay. In parallel, En-face immunohistochemical staining also showed increased expression of EC nitric oxide synthase (eNOS) along with increased levels of reactive oxygen species (ROS) and nitrotyrosine (NY) formation in OSS segments compared with USS. Conclusions: Together, our studies shed light on the early changes in EC response to acute induction of OSS and resulting down-regulation of EC mir-155, including; oxidative/inflammatory stress, EC dysfunction, loss of barrier function and cytoskeletal changes. Despite the early upregulation of eNOS, it could also potentially synergize with the activation of the RhoA-MYLK pathway in EC oxidative (ROS/NY)/inflammatory stress and associated EC dysfunction. Further studies are in progress to dissect the interplay between these different pathways and their causal relationships as downstream targets of EC miR-155.


2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Katherine Quigley ◽  
Karen Fang ◽  
Nelson Jen ◽  
Rongsong Li ◽  
Tzung Hsiai

Author(s):  
S. Yamada ◽  
H. Ito ◽  
M. Ishikawa ◽  
K. Yamamoto ◽  
M. Yamaguchi ◽  
...  

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