scholarly journals Activation of GPR30 with G1 inhibits oscillatory shear stress-induced adhesion of THP-1 monocytes to HAECs by increasing KLF2

Aging ◽  
2021 ◽  
Author(s):  
Chi Chen ◽  
Jingyan Chen ◽  
Xuefei Tao ◽  
Minghuan Fu ◽  
Biao Cheng ◽  
...  
Keyword(s):  
Shear Stress ◽  
Oscillatory Shear ◽  
Oscillatory Shear Stress

Abstract 561: Dysregulation of miR-155 in Acute Oscillatory Shear Stress (OSS)-mediated Oxidative Stress, Inflammation and Endothelial Dysfunction

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Islam Mohamed ◽  
Sheena Thomas ◽  
Kimberly Rooney ◽  
Roy Sutliff ◽  
Nick Willett ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Shear Stress ◽  
Barrier Function ◽  
Oscillatory Shear ◽  
Blue Dye ◽  
Down Regulation ◽  
Inflammatory Stress ◽  
Cytoskeleton Organization ◽  
Oscillatory Shear Stress

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.

scholarly journals MnSOD reduction causes mtDNA damage in HAEC under Oscillatory Shear Stress

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Katherine Quigley ◽  
Karen Fang ◽  
Nelson Jen ◽  
Rongsong Li ◽  
Tzung Hsiai
Keyword(s):  
Shear Stress ◽  
Oscillatory Shear ◽  
Mtdna Damage ◽  
Oscillatory Shear Stress

scholarly journals Quantification of Oscillatory Shear Stress from Reciprocating CSF Motion on 4D Flow Imaging

2021 ◽  
Author(s):  
S. Yamada ◽  
H. Ito ◽  
M. Ishikawa ◽  
K. Yamamoto ◽  
M. Yamaguchi ◽  
...  
Keyword(s):  
Shear Stress ◽  
Oscillatory Shear ◽  
Flow Imaging ◽  
4D Flow ◽  
Oscillatory Shear Stress ◽  
4D Flow Imaging

Abstract 363: Lim Domain Only 4 Is a Shear-Sensitive Protein, Playing a Critical Role in Endothelial Inflammation and Atherosclerosis

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Wakako Takabe ◽  
Chih-Wen Ni ◽  
Dong Ju Son ◽  
Noah Alberts-Grill ◽  
Hanjoong Jo
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Critical Role ◽  
Oscillatory Shear ◽  
Lim Domain ◽  
Disturbed Flow ◽  
Endothelial Inflammation ◽  
And Migration ◽  
Oscillatory Shear Stress ◽  
Stable Flow

Recently, we have shown that disturbed flow, characterized by low and oscillatory shear stress, caused by a partial ligation of mouse left carotid artery (LCA) rapidly induces atherosclerosis. Using the partial ligation model and genome-wide microarray study with aortic endothelial RNAs obtained directly from the flow-disturbed carotid arteries, we previously identified mechanosensitive genes in mouse endothelial RNA including LIM domain only 4 ( lmo4 ). Here we report that LMO4 is a shear-sensitive protein that regulates endothelial inflammation. Lmo4 was up-regulated by disturbed flow in mouse LCA compared to the contralateral right CA (RCA) exposed to stable flow. At protein levels, LMO4 expression was significantly higher not only in LCA in our surgical model but also in the lesser curvature (flow-disturbed and athero-prone region of mouse aortic arch) compared to the greater curvature (stable-flow and ather-protected region). In addition, immunohistochemical staining of LMO4 in human coronary arteries revealed that its expression is detectable only in intimal endothelial cells, but not in medial cells. While LMO4 is known as a potential oncogene and associated with growth, migration and invasion of breast cancer cells, its role in cardiovascular system is not known to our knowledge. We tested a hypothesis that LMO4 is a mechanosensitive gene and plays a critical role in regulation of endothelial cell biology. LMO4 protein expression was robustly induced by oscillatory shear stress (OS) compared to laminar shear (LS) in human umbilical vein endothelial cells (HUVEC). Treatment of HUVEC with siRNA against LMO4 significantly inhibited OS-induced inflammation and migration, but not apoptosis and cell cycle progression. Further, LMO4 siRNA treatment significantly blunted expression of VCAM-1 and interleukin-8 induced by OS in endothelial cells. These results suggest that LMO4 is a shear-induced gene that plays a critical role in OS-induced endothelial inflammation and migration, and potentially in atherosclerosis.

Juglanin suppresses oscillatory shear stress-induced endothelial dysfunction: An implication in atherosclerosis

2020 ◽  
Vol 89 ◽  
pp. 107048
Author(s):  
Jian Zhao ◽  
Xiaoqiang Quan ◽  
Zhouliang Xie ◽  
Leilei Zhang ◽  
Zhiwei Ding
Keyword(s):  
Shear Stress ◽  
Endothelial Dysfunction ◽  
Oscillatory Shear ◽  
Oscillatory Shear Stress

Integrated microfluidic chip for endothelial cells culture and analysis exposed to a pulsatile and oscillatory shear stress

Lab on a Chip ◽  
2009 ◽  
Vol 9 (21) ◽  
pp. 3118 ◽  
Author(s):  
Jianbo Shao ◽  
Lei Wu ◽  
Jianzhang Wu ◽  
Yunhuan Zheng ◽  
Hui Zhao ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Microfluidic Chip ◽  
Oscillatory Shear ◽  
Oscillatory Shear Stress

Non-Invasive Molecular Imaging of Shear Stress-Induced Endothelial Activation and Atherosclerotic Plaque Vulnerability

2012 ◽  
Author(s):  
K. Van der Heiden ◽  
H. C. Groen ◽  
P. C. Evans ◽  
L. Speelman ◽  
F. Gijsen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Atherosclerotic Lesion ◽  
Oscillatory Shear ◽  
Lesion Development ◽  
Non Invasive ◽  
Oscillatory Shear Stress ◽  
The Relationship ◽  
Atherosclerotic Lesion Development

Atherosclerosis is a lipid- and inflammation driven disease of the larger arteries and is found at specific locations in the arterial tree, i.e. at branches and bends where endothelial cells are exposed to low and low, oscillatory shear stress. Shear stress, the frictional force acting on the endothelial cells as a result of the blood flow, affects endothelial physiology. It determines the location of atherosclerotic lesion development as low and low, oscillatory shear stress induce pro-inflammatory transcription factors but reduce expression and/or activity of anti-inflammatory transcription factors in endothelial cells, rendering the vascular wall vulnerable for inflammation. Consequently, in the presence of atherosclerotic risk factors, such as hypercholesterolemia and diabetes, atherosclerotic lesion development can occur. Although the relationship between low and low, oscillatory shear stress and the prevalence of atherosclerosis has been recognized for several decades, insight into the mechanisms underlying this relationship is still incomplete. The correlation between shear stress and endothelial inflammation was demonstrated by in vitro experiments, in which cultured endothelial cells were exposed to specific flow profiles, and confirmed in vivo by gene expression pattern studies at atherosclerosis-susceptible sites. However, the relationship was not substantiated by direct causal in vivo evidence. Therefore, we developed a method to change the local shear stress field in mice in vivo and studied its effect on the endothelial molecular pathways and resulting atherosclerotic plaque formation. Moreover it allowed us to develop non-invasive molecular imaging strategies to detect vulnerable plaques.

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