Molecular and biological effects of hemodynamics on vascular cells

10.2741/1480 ◽  
2004 ◽  
Vol 9 (1-3) ◽  
pp. 3276 ◽  
Author(s):  
Sanjeev Pradhan
Keyword(s):  
Biological Effects ◽  
Vascular Cells

scholarly journals SARS-CoV-2 Spike Protein and Lung Vascular Cells

2020 ◽  
Vol 1 (1) ◽  
pp. 40-48
Author(s):  
Sri Jayalakshmi Suresh ◽  
Yuichiro Justin Suzuki
Keyword(s):  
Membrane Fusion ◽  
Viral Entry ◽  
Biological Effects ◽  
Spike Protein ◽  
Vascular Cells ◽  
Membrane Fusion Protein ◽  
Vascular Walls ◽  
Immunodeficiency Virus ◽  
Pulmonary Arterial

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is causing the current pandemic of coronavirus disease 2019 (COVID-19), and COVID-19 vaccines focus on its spike protein. However, in addition to facilitating the membrane fusion and viral entry, the SARS-CoV-2 spike protein promotes cell growth signaling in human lung vascular cells, and patients who have died of COVID-19 have thickened pulmonary vascular walls, linking the spike protein to a fatal disease, pulmonary arterial hypertension (PAH). In addition to SARS-CoV spike proteins, gp120, the viral membrane fusion protein of human immunodeficiency virus (HIV), has been reported to promote cell signaling, and long-term surviving HIV-positive patients have a high incidence of developing PAH. This article describes the findings of the SARS-CoV-2 spike protein affecting lung vascular cells and explains how the spike protein possibly increases the incidence of PAH. Since the SARS-CoV-2 spike protein will be administered to millions of people as COVID-19 vaccines, it is critical to understand the biological effects of this protein on human cells to ensure that it does not promote long-term adverse health consequences.

Abstract 564: Inflammasome-induced Endothelial Microparticles Exert Detrimental Effects on Recipient Vascular Cells

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Philipp Pfeifer ◽  
Sophia-Katharina Ebert ◽  
Lin Liu ◽  
Felix Jansen ◽  
Julian Jehle ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Biological Effects ◽  
Vascular Inflammation ◽  
Membrane Vesicles ◽  
Inflammasome Activation ◽  
Vascular Cells ◽  
Human Coronary Artery ◽  
Electron Microscopic ◽  
Endothelial Microparticles ◽  
Microscopic Imaging

Background: The inflammasome, a multi-protein signaling platform, is an important mediator of vascular inflammation resulting in atherosclerosis. Microparticles (MPs) are small membrane vesicles, specifically packaged and released from apoptotic cells for intercellular communication. Endothelial cell derived MPs have recently been linked to atherogenesis. Whether inflammasome activation in endothelial cells mediates MP release and thereby exert biological effects on recipient vascular cells is unknown. Methods and results: Human coronary artery endothelial cells (HCAEC) were primed with 1μg/ml LPS and subsequently stimulated with 20μM Nigericin leading to a specific inflammasome activation as detected by significant upregulation of Caspase-1 mRNA in RT-PCR and protein in Westernblots (Figure1). Inflammasome activation in vascular cells lead to formation of endothelial microparticles (EMP) in a time- and dosis-dependend manner (Figure 2). Comparison of EMP with beads of known size using flow cytometric and electron microscopic imaging could point out an EMP-size between 0,1 – 1 μm (Figure 3). EMP-uptake by recipient vascular cells could be illustrated by fluorescence-microscopic imaging of PKH26 labeled EMP (Figure 4). Viability assay and scratch assay showed detrimental effects of EMPs from inflammasome activated cells on recipient vascular cells. Viability, proliferation and migration were reduced significantly 4h after treatment (Figure 5). Conclusions: We show for the first time that Nigericin, an established inflammasome activator, leads to inflammasome activation and release of microparticles by endothelial cells. Furthermore, that these microparticles are taken up by recipient vascular cells and thereby cause cell death accompanied with reduced cell migration and proliferation.

scholarly journals Biological effects of fucoidan isolated from Fucus vesiculosus on thrombosis and vascular cells

2010 ◽  
Vol 45 (1) ◽  
pp. 51 ◽  
Author(s):  
Kyu-Won Kwak ◽  
Kil-Sang Cho ◽  
Ok-Jin Hahn ◽  
Kwang-Hyung Lee ◽  
Boo-Yong Lee ◽  
...  
Keyword(s):  
Biological Effects ◽  
Fucus Vesiculosus ◽  
Vascular Cells

Ultrastructural Changes in Three Different Mammalian Cells Following Ultraviolet Laser Irradiation

1972 ◽  
Vol 30 ◽  
pp. 350-351
Author(s):  
K. Shankar Narayan ◽  
Kailash C. Gupta ◽  
Tohru Okigaki
Keyword(s):  
Ultraviolet Light ◽  
Mammalian Cells ◽  
Biological Effects ◽  
Survival Rates ◽  
Chinese Hamster ◽  
Cell Types ◽  
Differential Sensitivity ◽  
Ultrastructural Changes ◽  
Ultraviolet Laser

The biological effects of short-wave ultraviolet light has generally been described in terms of changes in cell growth or survival rates and production of chromosomal aberrations. Ultrastructural changes following exposure of cells to ultraviolet light, particularly at 265 nm, have not been reported.We have developed a means of irradiating populations of cells grown in vitro to a monochromatic ultraviolet laser beam at a wavelength of 265 nm based on the method of Johnson. The cell types studies were: i) WI-38, a human diploid fibroblast; ii) CMP, a human adenocarcinoma cell line; and iii) Don C-II, a Chinese hamster fibroblast cell strain. The cells were exposed either in situ or in suspension to the ultraviolet laser (UVL) beam. Irradiated cell populations were studied either "immediately" or following growth for 1-8 days after irradiation.Differential sensitivity, as measured by survival rates were observed in the three cell types studied. Pattern of ultrastructural changes were also different in the three cell types.

Genomic analysis of C-type lectins

2002 ◽  
Vol 69 ◽  
pp. 59-72 ◽  
Author(s):  
Kurt Drickamer ◽  
Andrew J. Fadden
Keyword(s):  
Biological Effects ◽  
Cell Signalling ◽  
Genomic Analysis ◽  
Binding Activity ◽  
Immunoglobulin Superfamily ◽  
Carbohydrate Binding ◽  
Carbohydrate Recognition ◽  
Calcium Dependent ◽  
Binding Domains ◽  
Carbohydrate Recognition Domains

Many biological effects of complex carbohydrates are mediated by lectins that contain discrete carbohydrate-recognition domains. At least seven structurally distinct families of carbohydrate-recognition domains are found in lectins that are involved in intracellular trafficking, cell adhesion, cell–cell signalling, glycoprotein turnover and innate immunity. Genome-wide analysis of potential carbohydrate-binding domains is now possible. Two classes of intracellular lectins involved in glycoprotein trafficking are present in yeast, model invertebrates and vertebrates, and two other classes are present in vertebrates only. At the cell surface, calcium-dependent (C-type) lectins and galectins are found in model invertebrates and vertebrates, but not in yeast; immunoglobulin superfamily (I-type) lectins are only found in vertebrates. The evolutionary appearance of different classes of sugar-binding protein modules parallels a development towards more complex oligosaccharides that provide increased opportunities for specific recognition phenomena. An overall picture of the lectins present in humans can now be proposed. Based on our knowledge of the structures of several of the C-type carbohydrate-recognition domains, it is possible to suggest ligand-binding activity that may be associated with novel C-type lectin-like domains identified in a systematic screen of the human genome. Further analysis of the sequences of proteins containing these domains can be used as a basis for proposing potential biological functions.

Thrombin Augments Vascular Cell-dependent Migration of Human Mast Cells: Role of MGF

1997 ◽  
Vol 77 (03) ◽  
pp. 577-584 ◽  
Author(s):  
Mehrdad Baghestanian ◽  
Roland Hofbauer ◽  
Hans G Kress ◽  
Johann Wojta ◽  
Astrid Fabry ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Mast Cells ◽  
Umbilical Vein ◽  
Vascular Cells ◽  
Migratory Response ◽  
Thrombin Activation ◽  
Umbilical Vein Endothelial Cells ◽  
Primary Tissue ◽  
Local Expression

SummaryRecent data suggest that auricular thrombosis is associated with accumulation of mast cells (MC) in the upper endocardium (where usually no MC reside) and local expression of MGF (mast cell growth factor) (25). In this study, the role of vascular cells, thrombin-activation and MGF, in MC-migration was analyzed. For this purpose, cultured human auricular endocardial cells (HAUEC), umbilical vein endothelial cells (HUVEC) and uterine-(HUTMEC) and skin-derived (HSMEC) microvascular endothelial cells were exposed to thrombin or control medium, and the migration of primary tissue MC (lung, n = 6) and HMC-1 cells (human MC-line) against vascular cells (supernatants) measured. Supernatants (24 h) of unstimulated vascular cells (monolayers of endocardium or endothelium) as well as recombinant (rh) MGF induced a significant migratory response in HMC-1 (control: 3025 ± 344 cells [100 ± 11.4%] vs. MGF, 100 ng/ml: 8806 ± 1019 [291 ± 34%] vs. HAUEC: 9703 ± 1506 [320.8 ± 49.8%] vs. HUTMEC: 8950 ± 1857 [295.9 ± 61.4%] vs. HSMEC: 9965 ± 2018 [329.4 ± 66.7%] vs. HUVEC: 9487 ± 1402 [313.6 ± 46.4%], p <0.05) as well as in primary lung MC. Thrombin-activation (5 U/ml, 12 h) of vascular cells led to an augmentation of the directed migration of MC as well as to a hirudin-sensitive increase in MGF synthesis and release. Moreover, a blocking anti-MGF antibody was found to inhibit MC-migration induced by unstimulated or thrombin-activated vascular cells. Together, these data show that endocardial and other vascular cells can induce migration of human MC. This MC-chemotactic signal of the vasculature is associated with expression and release of MGF, augmentable by thrombin, and may play a role in the pathophysiology of (auricular) thrombosis.

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