Vascular endothelium Research Papers - Academia.edu (original) (raw)

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- Cognitive Science, Brain, Humans, Glioma
- by Martin Moser
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- Cytokines, Macrophages, Ischemia, Mice
- by Jorge Antonio Gamonal Aravena
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- Dentistry, Biology, Medicine, Biopsy
- by Edmund Garr
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- Biological Sciences, Pregnancy, Molecular and cellular biology, Humans

Endothelial-derived microparticles (EMPs) are a novel biological marker of endothelium injury and vasomotion disorders that are involved in pathogenesis of cardiovascular, metabolic, and inflammatory diseases. Circulating levels of EMPs are thought to reflect a balance between cell stimulation, proliferation, apoptosis, and cell death. Increased EMPs may be defined in several cardiovascular diseases, such as stable and unstable coronary artery disease, acute and chronic heart failure, hypertension, arrhythmias, thromboembolism, asymptomatic atherosclerosis as well as renal failure, metabolic disorders (including type two diabetes mellitus, abdominal obesity, metabolic syndrome, insulin resistance) and dyslipidemia. This review highlights the controversial opinions regarding impact of circulating EMPs in major cardiovascular and metabolic diseases and summarizes the perspective implementation of the EMPs in risk stratification models.

- by Alexander E Berezin
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- Biomarkers, Clinical Biochemistry, Risk assessment, Humans
- by Ronan Mullan
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- Inflammation, Rheumatoid Arthritis, Biopsy, Humans
- by Robert Hammer
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- Immunohistochemistry, Hypertension, Mice, Blood Pressure

Arginase 2 (Arg2) is a critical target in atherosclerosis because it controls endothelial nitric oxide, proliferation, fibrosis, and inflammation. Regulators of Arg2 transcription in the endothelium have not been characterized. The goal of the current study is to determine the role of specific histone deacetylases (HDACs) in the regulation of endothelial Arg2 transcription and endothelial function. The HDAC inhibitor trichostatin A increased levels of Arg2 mRNA, protein, and activity in both human aortic endothelial cells and mouse aortic rings. These changes occurred in both time- and dose-dependent patterns and resulted in Arg2-dependent endothelial dysfunction. Trichostatin A and the atherogenic stimulus oxidized low-density lipoprotein enhanced the activity of common promoter regions of Arg2. HDAC inhibition with trichostatin A also decreased endothelial nitric oxide, and these effects were blunted by arginase inhibition. Nonselective class I HDAC inhibitors enhanced Arg2 expres...

- by Gautam Sikka
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- RNA interference, Humans, Endothelial Cells, Mice
- by Weimin Guo
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- Cytokines, Real-time RT-PCR, Humans, NF-kappa B
- by Simon Bacon
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- Mechanical Engineering, Sports Medicine, Obesity, Diet
- by Fábio Mingatto
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- Animals, Male, Vascular endothelium, Rats
- by Makrina Savvidou
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- Ultrasound, Pregnancy, Humans, Female
- by annamaria naggi
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- Cancer, Breast Cancer, Treatment, Cell Adhesion
- by Federico Galvagni
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- Cell Migration, Morphogenesis, Gene Silencing, RNA interference
- by Filippo Drago and +2
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- Animal Behavior, Depression, Swimming, Serotonin
- by David Heimansohn
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- Endoscopy, Prospective studies, Humans, Smooth muscle
- by Béatrice Charreau
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- Apoptosis, Multidisciplinary, Gene Silencing, Signal Transduction
- by Yoshito Ikada
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- Regeneration, Wound Healing, Polymers, Elasticity

Pseudomonas aeruginosa, a common agent of septicemia, enters into human endothelial cellsin vitro but the effects of bacterial infection have not been addressed properly. In this study, human umbilical vein endothelial cells (HUVEC) were... more

- by Maria Cristina Assis
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- Microbiology, Immunology, Medical Microbiology, Transcription Regulation

The prodromal stage of atherosclerotic lesions is already formed during human fetal development. The presence of infections during childhood may increase synergistically the progression of atherogenesis. After delivery, especially those children exposed to severe maternal hypercholesterolemia should be followed up for the onset and development of acute and chronic infections and be included in clinical and noninvasive examinations of vascular function.

- by Orlando Pignalosa
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- Atherosclerosis, Medicine, Fetal development, Pregnancy
- by Michael Pepper
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- Genetics, Humans, Animals, Vascular endothelium
- by Paweena Susantitaphong
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- Kidney diseases, Polyamines, Humans, Female
- by O. Economou
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- Ultrasound Imaging, Treatment, Ultrasound, Humans
- by Günter Krämer
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- Face, Corticotropin Releasing Hormone, Humans, Male

Tubulointerstitial nephritis (TIN) antigen has been recently identified as a novel basement membrane macromolecule. It consists of a single chain of 58 kDa and exhibits a restricted distribution. The interaction between TIN antigen and laminin or type IV collagen has been studied using solid-phase binding assays and found to be for both macromolecules specific, saturable, and with an affinity in the low micromolar range. In similar assays, TIN antigen did not interact with heparin. In turbidimetry assays, it was found that the presence of TIN antigen did not affect the polymerization of type IV collagen but had a concentration-dependent inhibitory effect on laminin polymerization and on preformed laminin polymers. TIN antigen was able to promote adhesion of epithelial cells derived from kidney tubules and of endothelial cells derived from aorta. The data suggest that TIN antigen may be a macromolecule of importance both for basement membrane ultrastructure and cellular adhesion.

- by Ralph Butkowski
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- Kinetics, Cell Adhesion, Biological Chemistry, Biological Sciences
- by Apostolos Armaganidis
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- Adolescent, Pulmonary Hypertension, Humans, Capillaries
- by Daniel Green
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- Environmental Psychology, Obesity, Treatment Outcome, Ultrasound
- by Hiroyuki Miyachi
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- Organic Chemistry, Cell line, In Vitro, Humans

Salmosin is a snake venom-derived novel disintegrin that antagonizes platelet aggregation. In this study, we investigated its functional specificity in tumor angiogenesis. Salmosin significantly inhibited bovine capillary endothelial cell proliferation induced by basic fibroblast growth factor but had no effect on normal growth of the cell. The basic fibroblast growth factor-induced in vivo angiogenesis in the chorioallantoic membrane was disrupted by salmosin treatment without affecting normal embryonic angiogenesis. Adhesion of the bovine capillary endothelial cells to vitronectin was also inhibited by the binding of salmosin to the alpha(v)beta3 integrin. Both the metastatic-tumor growth and the solid-tumor growth that developed in mice were effectively suppressed by salmosin treatment. Several lines of experimental evidence strongly suggest that the tumor-specific antiangiogenic activity of salmosin disrupts tumor growth by blocking the alpha(v)beta3 integrin that is expressed o...

- by 영돈 이
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- Cancer, Cell Adhesion, Mice, Animals

It has been suggested that transforming growth factor-beta1 (TGF-beta1) plays an important role in the pathogenesis of diabetes-induced erectile dysfunction. To investigate the expression and activity of Smad transcriptional factors, the key molecules for the initiation of TGF-beta-mediated fibrosis, in the penis of streptozotocin (STZ)-induced diabetic rats. Fifty-two 8-week-old Sprague-Dawley rats were used and divided into control and diabetic groups. Diabetes was induced by an intravenous injection of STZ. Eight weeks later, erectile function was measured by electrical stimulation of the cavernous nerve (N = 12 per group). The penis was harvested and stained with Masson trichrome or antibody to TGF-beta1, phospho-Smad2 (P-Smad2), smooth muscle alpha-actin, and factor VIII (N = 12 per group). Penis specimens from a separate group of animals were used for TGF-beta1 enzyme-linked immunosorbent assay (ELISA), P-Smad2/Smad2, phospho-Smad3 (P-Smad3)/Smad3, fibronectin, collagen I, and collagen IV western blot, or hydroxyproline determination. Erectile function was significantly reduced in diabetic rats compared with that in controls. The expression of TGF-beta1, P-Smad2, and P-Smad3 protein evaluated by ELISA or western blot was higher in diabetic rats than in controls. Compared with that in control rats, P-Smad2 expression was higher mainly in smooth muscle cells and fibroblasts of diabetic rats, whereas no significant differences were noted in endothelial cells or in the dorsal nerve bundle. Cavernous smooth muscle and endothelial cell contents were lower in diabetic rats than in controls. Cavernous fibronectin, collagen IV, and hydroxyproline content was significantly higher in diabetic rats than in controls. Upregulation of TGF-beta1 and activation of the Smad signaling pathway in the penis of diabetic rats might play important roles in diabetes-induced structural changes and deterioration of erectile function.

- by Seok Park
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- Erectile dysfunction, Signal Transduction, Sexual Medicine, Animals
- by Anne-elen Kernaleguen and +1
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- Regeneration, Atherosclerosis, Apoptosis, Cell Division

Vascular endothelial growth factor (VEGF) is a potent regulator of angiogenesis, which exerts direct effects on vascular endothelial cells, including endothelial cell proliferation and survival, tubulogenesis, and vascular permeability. In this study, we examined whether Neovastat, a naturally occurring multifunctional antiangiogenic drug, could inhibit the endothelial cell response to VEGF stimulation. We demonstrated that Neovastat was able to block the VEGF-dependent microvessel sprouting from Matrigel-embedded rat aortic rings, and it also blocked the VEGF-induced endothelial cell tubulogenesis in vitro. In vivo studies showed that Neovastat was able to specifically inhibit VEGF-induced plasma extravasation in numerous tissues, including pancreas and skin. The mechanism of action of Neovastat on VEGF-mediated effects was also evaluated at the molecular level. Neovastat was shown to compete against the binding of VEGF to its receptor in endothelial cells and significantly inhibit...

- by Pierre Sirois and +3
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- Cell Division, Humans, Capillaries, Animals
- by G. Plotnick
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- Treatment, Humans, Male, Exploration
- by Jassim Al Suwaidi
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- Obesity, Adolescent, Multivariate Analysis, Adenosine
- by Martin Feelisch
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- Free Radicals, Ultrasound, Cardiovascular disease, Free Radical
- by Valmore Bermudez
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- Drug interactions, Dopamine, Lipids, Humans
- by Andrew Falconar
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- Dengue Virus, Biological Sciences, Platelet, Fibrinogen
- by Dragomir N Serban
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- Animals, Male, Vascular endothelium, Activity
- by Oscar Infante
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- Cardiology, Echocardiography, Heart Failure, Humans
- by Gary Reynolds
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- Immunology, Immunology of the Gut, Dendritic Cells, Humans
- by Marc Hoylaerts
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- Molecular Medicine, Gene Therapy, Atherosclerosis, Cardiovascular disease
- by Rosemarie Lichtner and +1
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- Kinetics, Cell Adhesion, Extracellular Matrix, Cytoskeleton
- by Stephen Squinto
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- Immunology, Complement activation, Molecular, Molecular Immunology
- by John Mayer
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- Tissue Engineering, Sheep, Animals, Plant tissue Culture Techniques
- by Jing-jy Cheng
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- Engineering, Cell Adhesion, Gene expression, Lipopolysaccharide

Neutrophil collagenase (matrix metalloproteinase-8 or MMP-8) is regarded as being synthesized exclusively by polymorphonuclear neutrophils (PMN). However, in vivo MMP-8 expression was observed in mononuclear fibroblast-like cells in the rheumatoid synovial membrane. In addition, we detected MMP-8 mRNA expression in cultured rheumatoid synovial fibroblasts and human endothelial cells. Up-regulation of MMP-8 was observed after treatment of the cells with either tumor necrosis factor-alpha (10 ng/ml) or phorbol 12-myristate 13-acetate (10 nM). Western analysis showed a similar regulation at the protein level. The size of secreted MMP-8 was 50 kDa, which is about 30 kDa smaller than MMP-8 from PMN. Conditioned media from rheumatoid synovial fibroblasts contained both type I and II collagen degrading activity. However, degradation of type II collagen, but not that of type I collagen, was completely inhibited by 50 microM doxycycline, suggesting specific MMP-8 activity. In addition, doxycycline down-regulated MMP-8 induction, at both the mRNA and protein levels. Thus MMP-8 exerts markedly wider expression in human cells than had been thought previously, implying that PMN are not the only source of cartilage degrading activity at arthritic sites. The inhibition of both MMP-8 activity and synthesis by doxycycline provides an incentive for further studies on the clinical effects of doxycycline in the treatment of rheumatoid arthritis.

- by Meeri Sutinen
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- Catalysis, Rheumatoid Arthritis, Enzyme Inhibitors, Biological Chemistry
- by Arnold Reuser
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- Electron Microscopy, Skeletal muscle biology, Treatment Outcome, Humans

Interaction of fibrin with endothelial cells through their receptor VE-cadherin has been implicated in modulation of angiogenesis and inflammation. Previous studies identified the VE-cadherin-binding site in the fibrin βN-domains formed by the NH2-terminal regions of fibrin β chains, and revealed that the recombinant dimeric (β15-66)2 fragment mimicking these domains preserves the VE-cadherin-binding properties of fibrin. To test if the other fibrin(ogen) regions/domains are involved in this interaction and localize the complementary fibrin-binding site in VE-cadherin, we prepared several recombinant fragments containing individual extracellular domains of VE-cadherin or combinations thereof, as well as several fragments corresponding to various fibrin(ogen) regions, and tested the interactions between them by ELISA and surface plasmon resonance. The experiments revealed that the βN-domains are the only fibrin(ogen) regions involved in the interaction with VE-cadherin. They also loc...

- by Leonid Medved
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- Biochemistry, Kinetics, Fibrinogen, Fibrin