scholarly journals Silicon microgrooves for contact guidance of human aortic endothelial cells

2017 ◽  
Vol 8 ◽  
pp. 675-681 ◽  
Author(s):  
Sara Fernández-Castillejo ◽  
Pilar Formentín ◽  
Úrsula Catalán ◽  
Josep Pallarès ◽  
Lluís F Marsal ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Cellular Response ◽  
Cytotoxic Effect ◽  
Contact Guidance ◽  
Silicon Substrates ◽  
Aortic Endothelial Cells ◽  
Human Aortic Endothelial Cells ◽  
Microscopy Images ◽  
Aortic Endothelial

Background: Micro- and nanoscale substrates have been fabricated in order to study the influence of the topography on the cellular response. The aim of this work was to prepare different collagen-coated silicon substrates displaying grooves and ridges to mimic the aligned and elongated endothelium found in linear vessels, and to use them as substrates to study cell growth and behaviour. Results: The influence of groove-shaped substrates on cell adhesion, morphology and proliferation were assessed, by comparing them to flat silicon substrates, used as control condition. Using human aortic endothelial cells, microscopy images demonstrate that the cellular response is different depending on the silicon surface, when it comes to cell adhesion, morphology (alignment, circularity and filopodia presence) and proliferation. Moreover, these structures exerted no cytotoxic effect. Conclusion: The results suggest that topographical patterning influences cell response. Silicon groove substrates can be used in developing medical devices with microscale features to mimic the endothelium in lineal vessels.

Infection with a periodontal pathogen increases mononuclear cell adhesion to human aortic endothelial cells

2007 ◽  
Vol 190 (2) ◽  
pp. 271-281 ◽  
Author(s):  
Georg A. Roth ◽  
Bernhard Moser ◽  
Franziska Roth-Walter ◽  
Mary Beth Giacona ◽  
Evis Harja ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Mononuclear Cell ◽  
Periodontal Pathogen ◽  
Aortic Endothelial Cells ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

scholarly journals Inhibitive Effects of Mulberry Leaf-Related Extracts on Cell Adhesion and Inflammatory Response in Human Aortic Endothelial Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
P.-Y. Chao ◽  
K.-H. Lin ◽  
C.-C. Chiu ◽  
Y.-Y. Yang ◽  
M.-Y. Huang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Dna Binding ◽  
Human Lymphocytes ◽  
Trolox Equivalent Antioxidant Capacity ◽  
Peroxisome Proliferator ◽  
Aortic Endothelial Cells ◽  
Mulberry Leaf ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

Effects of mulberry leaf-related extracts (MLREs) on hydrogen peroxide-induced DNA damage in human lymphocytes and on inflammatory signaling pathways in human aortic endothelial cells (HAECs) were studied. The tested MLREs were rich in flavonols, especially bombyx faces tea (BT) in quercetin and kaempferol. Polyphenols, flavonoids, and anthocyanidin also abounded in BT. The best trolox equivalent antioxidant capacity (TEAC) was generated from the acidic methanolic extracts of BT. Acidic methanolic and water extracts of mulberry leaf tea (MT), mulberry leaf (M), and BT significantly inhibited DNA oxidative damage to lymphocytes based on the comet assay as compared to the H2O2-treated group. TNF-α-induced monocyte-endothelial cell adhesion was significantly suppressed by MLREs. Additionally, nuclear factor kappa B (NF-κB) expression was significantly reduced by BT and MT. Significant reductions were also observed in both NF-κB and activator protein (AP)-1 DNA binding by MLREs. Significant increases in peroxisome proliferator-activated receptor (PPAR)αandγDNA binding by MLREs were also detected in M and MT extracts, but no evidence for PPARαDNA binding in 50 μg/mL MT extract was found. Apparently, MLREs can provide distinct cytoprotective mechanisms that may contribute to its putative beneficial effects on suppressing endothelial responses to cytokines during inflammation.

scholarly journals Collagen-mimetic hydrogels promote human endothelial cell adhesion, migration and phenotypic maturation

2015 ◽  
Vol 3 (40) ◽  
pp. 7912-7919 ◽  
Author(s):  
Dany J. Munoz-Pinto ◽  
Viviana R. Guiza-Arguello ◽  
Silvia M. Becerra-Bayona ◽  
Josh Erndt-Marino ◽  
Satyavrata Samavedi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Endothelial Cell ◽  
Human Endothelial Cell ◽  
Aortic Endothelial Cells ◽  
Hydrogel Coatings ◽  
Human Aortic Endothelial Cells ◽  
Endothelial Cell Adhesion ◽  
Aortic Endothelial

This work evaluates the response of human aortic endothelial cells (HAECs) to thromboresistant collagen-mimetic hydrogel coatings.

scholarly journals Identification of Phenotypic Modulation of Angiotensin-(1-7) in Thrombin-Stimulated Human Aortic Endothelial Cells from iTRAQ Quantitative Proteomics

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 4999-4999
Author(s):  
Ching-Tien Peng ◽  
Kang-Hsi Wu
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Conflicts Of Interest ◽  
Critical Role ◽  
Aortic Endothelial Cells ◽  
Regulatory Pathways ◽  
Ras Activation ◽  
Cytoskeleton Remodeling ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

Abstract Introduction: The primary effector of renin-angiotensin system (RAS) system is angiotensin II. RAS activation causes many detrimental effects via AT1 receptor. Angiotensin-(1-7)/ angiotensin-converting enzyme 2/Mas axis is a newly identified counter-regulatory pathway against RAS system. Thrombin plays a critical role in coagulation and inflammation processes in vascular endothelium. Although RAS activation is associated with thrombotic complications, it is unknown whether angiotensin-(1-7) can modulate the pleotropic effects of thrombin. In this study, we investigate the proteomic changes of angiotensin-(1-7) effects on thrombin-stimulated human aortic endothelial cells (HAECs). Materials and methods: HAECs were pretreated with 10-7M anigotenion-(1-7) for 1 h and stimulated with 2 units/mL thrombin for additional 5 h. Their proteomes were investigated using isobaric tags for the relative and absolute quantification (iTRAQ) and MetaCoreTMsoftware. Results: A total of 653, 717 and 801 proteins were identified in triplicated iTRAQ analyses. MetaCoreTM pathway analysis identified that iTRAQ data showed the consistent pathway alterations (70%) in triplicated experiments. The same altered pathways included "Cytoskeleton remodeling_Cytoskeleton remodeling", "Cell adhesion_Integrin-mediated cell adhesion and migration", "Cell adhesion_Chemokines and adhesion" , "Cytoskeleton remodeling _ Regulation of actin cytoskeleton by Rho GTPases", "LRRK2 in neurons in Parkinson's disease", "Cytoskeleton remodeling_Fibronectin-binding integrins in cell motility", "Cytoskeleton remodeling _TGF, WNT and cytoskeletal remodeling" were among the top 10 statistically significant pathways. Additional experiments validated the phenotypes of angiotensin-(1-7) effects in thrombin-stimulated HAECs. Conclusions: Several regulatory pathways are altered by angiotensin-(1-7) in thrombin-stimulated HAECs, with cytoskeleton remodeling, cell adhesion and cell migration (motility) as the dominant altered phenotypes. Disclosures No relevant conflicts of interest to declare.

CRP promotes monocyte-endothelial cell adhesion via Fcγ receptors in human aortic endothelial cells under static and shear flow conditions

2006 ◽  
Vol 291 (3) ◽  
pp. H1170-H1176 ◽  
Author(s):  
Sridevi Devaraj ◽  
Benjamin Davis ◽  
Scott I. Simon ◽  
Ishwarlal Jialal
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Endothelial Cell ◽  
Shear Flow ◽  
Fcγ Receptors ◽  
Aortic Endothelial Cells ◽  
Static Conditions ◽  
Human Aortic Endothelial Cells ◽  
Endothelial Cell Adhesion ◽  
Aortic Endothelial

Monocyte-endothelial cell adhesion is a key early event in atherogenesis. C-reactive protein (CRP), a cardiovascular risk marker, is known to stimulate ICAM and VCAM in human aortic endothelial cells (HAEC) and induces monocyte-endothelial cell adhesion. In this study, we examined the mechanisms by which native CRP promotes monocyte-endothelial cell adhesion under static conditions and tested the effect of CRP on adhesion under shear flow. Incubation of HAEC with CRP (>25 μg/ml) upregulated NF-κB activity, and this resulted in a significant increase in ICAM (54% increase, P < 0.001), VCAM (41% increase, P < 0.01), and monocyte-endothelial cell adhesion (44% increase, P < 0.02) compared with those of control. Preincubation with antibodies to CD32 and CD64 but not CD16 effectively inhibited this activation. Blocking NF-κB activity with inhibitors or a dominant negative inhibitory κB significantly decreased ICAM, VCAM upregulation, and subsequent monocyte-endothelial cell adhesion. Preincubation with antibodies to CD32 and CD64 or transient transfection with small interference RNA to CD32 attenuated CRP-induced NF-κB activity, ICAM, VCAM, and monocyte-endothelial cell adhesion under static conditions. Also, the Syk kinase inhibitor piceatannol and MG-132, a proteasome degradation inhibitor, produced similar attenuation in NF-κB activity, ICAM, VCAM, and adhesion. Furthermore, CRP-activated endothelial cells supported monocyte rolling, arrest, and transmigration in shear flow (2 dyn/cm2), and this was also inhibited by preincubation with antibodies to CD32 and CD64. Thus, in HAEC, CRP upregulates monocyte-endothelial adhesion by activation of NF-κB through engaging the Fcγ receptors CD32 and CD64.

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