A5102877904- Cell Adhesion Molecules Research
- Angiogenesis and VEGF in Cancer
- MicroRNA in disease regulation
- Atherosclerosis and Cardiovascular Diseases
- Coronary Interventions and Diagnostics
- Cellular Mechanics and Interactions
- TGF-β signaling in diseases
- Circular RNAs in diseases
- Cancer-related molecular mechanisms research
- Bone Metabolism and Diseases
- Nitric Oxide and Endothelin Effects
- Kruppel-like factors research
- Hippo pathway signaling and YAP/TAZ
- Peroxisome Proliferator-Activated Receptors
- Epigenetics and DNA Methylation
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Cardiovascular Health and Disease Prevention
- Histone Deacetylase Inhibitors Research
- Fluid Dynamics and Turbulent Flows
- Protease and Inhibitor Mechanisms
- Peripheral Artery Disease Management
- Mesenchymal stem cell research
- Platelet Disorders and Treatments
- Electrospun Nanofibers in Biomedical Applications
- Protein Kinase Regulation and GTPase Signaling
National Health Research Institutes
2015-2025
Taipei Medical University
2017-2025
National Tsing Hua University
2012-2024
National Taiwan University
1997-2021
Institute of Cell Biology
2019
National Cheng Kung University
1992-2018
National Taiwan University Hospital
2018
University of California, San Diego
2003-2015
La Jolla Bioengineering Institute
2009-2015
Peking University
2015
Adhesion of circulating monocytes to vascular endothelial cells (ECs) is a critical event leading inflammation and, hence, development atherosclerosis. MicroRNAs (miRs) are class endogenous, highly conserved, noncoding small RNAs that play important roles in regulating gene expression and cellular function, as well pathogenesis Here, we showed oscillatory shear stress (OSS) induces the miR-21 at transcriptional level cultured human umbilical vein ECs via an increased binding c-Jun, which...
Rationale: Endothelial microRNA-126 (miR-126) modulates vascular development and angiogenesis. However, its role in the regulation of smooth muscle cell (SMC) function is unknown. Objective: To elucidate miR-126 secreted by endothelial cells (ECs) regulating SMC turnover vitro vivo, as well effects shear stress on regulation. Methods Results: Coculture SMCs with ECs or treatment conditioned media from static EC monoculture (EC-CM) increased level turnover; these were abolished inhibition...
Objective— Vascular endothelial cells (ECs) are subjected to shear stress and cytokine stimulation. We studied the interplay between in modulating expression of adhesion molecule genes ECs. Methods Results— Shear (20 dynes/cm 2 ) was applied ECs prior and/or following addition tumor necrosis factor (TNF)-α. increased TNF-α–induced intercellular molecule-1 (ICAM-1) at both mRNA surface protein levels, but decreased vascular (VCAM-1) E-selectin. Transfection studies using promoter reporter...
Atherosclerotic lesions tend to localize at curvatures and branches of the arterial system, where local flow is often disturbed irregular (e.g., separation, recirculation, complex patterns, nonuniform shear stress distributions). The effects such conditions on cultured human umbilical vein endothelial cells (HUVECs) were studied in vitro by using a vertical-step channel (VSF). Detailed distributions structures have been computed finite volume method general curvilinear coordinate system....
Abstract Vascular endothelial cells (ECs) are constantly subjected to flow-induced shear stress. Although the effects of stress on ECs well known, intracellular signal mechanisms remain largely unclear. Reactive oxygen species (ROS) have recently been suggested act as second messengers. The potential role ROS in shear-induced gene expression was examined present study by subjecting a force using parallel-plate flow chamber system. under increased their indicated superoxide production. This...
Interstitial flow in and around tumor tissue affects the mechanical microenvironment to modulate cell growth metastasis. We investigated roles of flow-induced shear stress modulating cycle distribution four lines underlying mechanisms. In all lines, incubation under static conditions for 24 or 48 h led G(0)/G(1) arrest; contrast, (12 dynes/cm(2)) induced G(2)/M arrest. The molecular basis effect was analyzed, presentation on mechanism is focused human MG63 osteosarcoma cells. Shear increased...
Endothelial proliferation, which is an important process in vascular homeostasis, can be regulated by the extracellular microenvironment. In this study we demonstrated that proliferation of endothelial cells (ECs) was enhanced on hydrogels with high stiffness (HSG, 21.5 kPa) comparison to those low (LSG, 1.72 kPa). ECs HSG showed markedly prominent stress fibers and a higher RhoA activity than LSG. Blockade attenuated fiber formation HSG, but had little effect LSG; enhancement opposite...
Vascular endothelial cells (ECs) are exposed to different flow patterns (i.e., disturbed vs. laminar), and the associated oscillatory shear stress (OSS) or pulsatile (PSS) lead differential responses. We investigated roles of class I II histone deacetylases (HDAC-1/2/3 HDAC-5/7, respectively) in regulating NF-E2–related factor-2 (Nrf2) Krüppel-like (KLF2), two transcription factors governing many shear-responsive genes, cell cycle ECs response OSS. Application OSS (0.5 ± 4 dynes/cm 2 )...
Intracellular reactive oxygen species (ROS) may participate in cellular responses to various stimuli including hemodynamic forces and act as signal transduction messengers. Human umbilical vein endothelial cells (ECs) were subjected laminar shear flow with stress of 15, 25, or 40 dynes/cm2 a parallel plate chamber demonstrate the potential role ROS shear-induced response. The use 2′,7′-dichlorofluorescin diacetate (DCFH-DA) measure levels ECs indicated that for 15 minutes resulted 0.5-...
Vascular endothelial cells (ECs) are constantly exposed to blood flow-induced shear stress, but the mechanism of force-specific activation their signaling modulate cellular function remains unclear. We have demonstrated that bone morphogenetic protein receptor (BMPR)-specific Smad1/5 can be force-specifically activated by oscillatory stress (OSS) in ECs cause cell cycle progression. is highly atherosclerotic lesions diseased human coronary arteries from patients with end-stage heart failure...
Rationale : Phenotypic modulation of smooth muscle cells (SMCs), which are located in close proximity to endothelial (ECs), is critical regulating vascular function. The role flow-induced shear stress the SMC phenotype has not been well defined. Objective objective was elucidate on ECs modulating and its underlying mechanism. Methods Results Application (12 dyn/cm 2 ) cocultured with SMCs modulated from synthetic contractile state, upregulation markers, downregulation proinflammatory genes,...
Disturbed blood flow at arterial branches and curvatures modulates endothelial function predisposes the region to inflammation subsequent development of atherosclerotic lesions. Activation Toll-like receptors (TLRs), in particular TLR4, contributes vascular inflammation. Therefore, we investigate whether TLR4 can sense disturbed (DF) mediate inflammation.En face staining endothelium revealed that expression, activation, its downstream inflammatory markers were elevated mouse aortic arch...
Abstract In type 1 and 2 diabetes mellitus, increased cardiac fibrosis, stiffness associated diastolic dysfunction may be the earliest pathological phenomena in diabetic cardiomyopathy. Endothelial‐mesenchymal transition (EndMT) endothelia cells (ECs) is a critical cellular phenomenon that increases fibroblasts (CFs) fibrosis hearts. The purpose of this paper to explore molecular mechanism miR‐21 regulating EndMT perivascular vivo, hyperglycaemia up‐regulated mRNA level , aggravated collagen...
Atherosclerotic complications represent the leading cause of cardiovascular mortality globally. Dysfunction endothelial cells (ECs) often initiates pathological events in atherosclerosis. In this study, we sought to investigate transcriptional profile atherosclerotic aortae, identify novel regulator dysfunctional ECs and hence provide mechanistic insights into progression. We applied single-cell RNA sequencing (scRNA-seq) on aortic from Western diet-fed apolipoprotein E-deficient (ApoE−/−)...
Abstract —Endothelial cells (ECs) subjected to shear stress constantly release nitric oxide (NO). The effect of NO on stress–induced endothelial responses was examined. ECs induced a transient and force–dependent increase in early growth response-1 (Egr-1) mRNA levels. Treatment with an donor, S -nitroso- N -acetylpenicillamine (SNAP) or 3-morpholinosydnonimine (SIN-1), inhibited this Egr-1 expression. Conversely, synthase inhibitor ECs, G -monomethyl- l -arginine, augmented modulation...