The protective effects of azilsartan against oscillatory shear stress‐induced endothelial dysfunction and inflammation are mediated by KLF6

2021 ◽  
Author(s):  
Guoqian Wei ◽  
Dayong Zhu ◽  
Yongtao Sun ◽  
Lan Zhang ◽  
Xian Liu ◽  
...  
Keyword(s):  
Shear Stress ◽  
Endothelial Dysfunction ◽  
Oscillatory Shear ◽  
Protective Effects ◽  
Oscillatory Shear Stress

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

Plaque-prone hemodynamics impair endothelial function in pig carotid arteries

2006 ◽  
Vol 290 (6) ◽  
pp. H2320-H2328 ◽  
Author(s):  
Veronica Gambillara ◽  
Céline Chambaz ◽  
Gabriela Montorzi ◽  
Sylvain Roy ◽  
Nikos Stergiopulos ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Endothelial Cells ◽  
Shear Stress ◽  
Endothelial Dysfunction ◽  
Oscillatory Shear ◽  
Enos Gene ◽  
Low Shear Stress ◽  
Oscillatory Shear Stress ◽  
Low Shear

Hemodynamic forces play an active role in vascular pathologies, particularly in relation to the localization of atherosclerotic lesions. It has been established that low shear stress combined with cyclic reversal of flow direction (oscillatory shear stress) affects the endothelial cells and may lead to an initiation of plaque development. The aim of the study was to analyze the effect of hemodynamic conditions in arterial segments perfused in vitro in the absence of other stimuli. Left common porcine carotid segments were mounted into an ex vivo arterial support system and perfused for 3 days under unidirectional high and low shear stress (6 ± 3 and 0.3 ± 0.1 dyn/cm2) and oscillatory shear stress (0.3 ± 3 dyn/cm2). Bradykinin-induced vasorelaxation was drastically decreased in arteries exposed to oscillatory shear stress compared with unidirectional shear stress. Impaired nitric oxide-mediated vasodilation was correlated to changes in both endothelial nitric oxide synthase (eNOS) gene expression and activation in response to bradykinin treatment. This study determined the flow-mediated effects on native tissue perfused with physiologically relevant flows and supports the hypothesis that oscillatory shear stress is a determinant factor in early stages of atherosclerosis. Indeed, oscillatory shear stress induces an endothelial dysfunction, whereas unidirectional shear stress preserves the function of endothelial cells. Endothelial dysfunction is directly mediated by a downregulation of eNOS gene expression and activation; consequently, a decrease of nitric oxide production and/or bioavailability occurs.

scholarly journals G3BP2 regulates oscillatory shear stress-induced endothelial dysfunction

2021 ◽  
Author(s):  
Tianhan Li ◽  
Juhui Qiu ◽  
Tingting Jia ◽  
Yinming Liang ◽  
Kun Zhang ◽  
...  
Keyword(s):  
Shear Stress ◽  
Endothelial Dysfunction ◽  
Oscillatory Shear ◽  
Oscillatory Shear Stress

scholarly journals Oscillatory Shear Stress Induces Endothelial Dysfunction through the Activation of P2Y12

2019 ◽  
Vol 16 (S2) ◽  
pp. 142-142
Author(s):  
Jianxiong Xu ◽  
Lu Wang ◽  
Jinxuan Wang ◽  
Juhui Qiu ◽  
Guixue Wang
Keyword(s):  
Shear Stress ◽  
Endothelial Dysfunction ◽  
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.

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