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Article ; Online: Alcohol and vascular endothelial function: Biphasic effect highlights the importance of dose.

Rajendran, Naresh K / Liu, Weimin / Cahill, Paul A / Redmond, Eileen M

Alcohol, clinical & experimental research

2023 Volume 47, Issue 8, Page(s) 1467–1477

Abstract: Background: Alcohol (ethanol) consumption has different influences on arterial disease, being protective or harmful depending on the amount and pattern of consumption. The mechanisms mediating these biphasic effects are unknown. Whereas endothelial ... ...

Abstract	Background: Alcohol (ethanol) consumption has different influences on arterial disease, being protective or harmful depending on the amount and pattern of consumption. The mechanisms mediating these biphasic effects are unknown. Whereas endothelial cells play a critical role in maintaining arterial health, this study compared the effects of moderate and high alcohol concentrations on endothelial cell function. Methods: Human coronary artery endothelial cells (HCAEC) were treated with levels of ethanol associated with either low-risk/moderate drinking (i.e., 25 mM) or high-risk/heavy drinking (i.e., 50 mM) after which endothelial function was assessed. The effect of ethanol's primary metabolite acetaldehyde (10 and 25 μM) was also determined. Results: Moderate ethanol exposure (25 mM) improved HCAEC barrier integrity as determined by increased transendothelial electrical resistance (TEER), inhibited cell adhesion molecule (CAM) mRNA expression, decreased inflammatory cytokine (interferon-γ and interleukin 6) production, inhibited monocyte chemotactic protein-1 (MCP-1) expression and monocyte adhesion, and increased homeostatic Notch signaling. In contrast, exposure to high-level ethanol (50 mM) decreased TEER, increased CAM expression and inflammatory cytokine production, and stimulated MCP-1 and monocyte adhesion, with no effect on Notch signaling. Reactive oxygen species (ROS) generation and endothelial nitric oxide synthase activity were increased by both alcohol treatments, and to a greater extent in the 50 mM ethanol group. Acetaldehyde-elicited responses were generally the same as those of the high-level ethanol group. Conclusions: Ethanol has biphasic effects on several endothelial functions such that a moderate level maintains the endothelium in a nonactivated state, whereas high-level ethanol causes endothelial dysfunction, as does acetaldehyde. These data show the importance of dose when considering ethanol's effects on arterial endothelium, and could explain, in part, the J-shaped relationship between alcohol concentration and atherosclerosis reported in some epidemiologic studies.
Language	English
Publishing date	2023-07-10
Publishing country	United States
Document type	Journal Article
ISSN	2993-7175
ISSN (online)	2993-7175
DOI	10.1111/acer.15138
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Caveolin-1 inhibition mediates the opposing effects of alcohol on γ-secretase activity in arterial endothelial and smooth muscle cells.

Rajendran, Naresh K / Liu, Weimin / Cahill, Paul A / Redmond, Eileen M

Physiological reports

2023 Volume 11, Issue 1, Page(s) e15544

Abstract: Notch is important to vessel homeostasis. We investigated the mechanistic role of caveolin-1 (Cav-1) in mediating the effects of alcohol (Ethanol/EtOH) on the γ-secretase proteolytic activity necessary for Notch signaling in vascular cells. Human ... ...

Abstract	Notch is important to vessel homeostasis. We investigated the mechanistic role of caveolin-1 (Cav-1) in mediating the effects of alcohol (Ethanol/EtOH) on the γ-secretase proteolytic activity necessary for Notch signaling in vascular cells. Human coronary artery endothelial cells (HCAEC) were treated with EtOH (0-50 mM), Notch ligand delta-like ligand 4 (Dll4), and the γ-secretase inhibitor DAPT. EtOH stimulated Notch signaling in HCAEC as evidenced by increased Notch receptor (N1, N4) and target gene (hrt2, hrt3) mRNA levels with the most robust response achieved at 25 mM EtOH. Ethanol (25 mM) stimulated γ-secretase proteolytic activity, to the same extent as Dll4, in HCAEC membranes. Ethanol inhibited Cav-1 mRNA and protein levels in HCAEC. Caveolin-1 negatively regulated γ-secretase activity in HCAEC as Cav-1 knockdown stimulated it, while Cav-1 overexpression inhibited it. Moreover, Cav-1 overexpression blocked the stimulatory effect of EtOH on γ-secretase activity in HCAEC. Although EtOH also inhibited Cav-1 expression in human coronary artery smooth muscle cells (HCASMC), EtOH inhibited γ-secretase activity in HCASMC in contrast to its effect in HCAEC. The inhibitory effect of EtOH on γ-secretase in HCASMC was mimicked by Cav-1 knockdown and prevented by Cav-1 overexpression, suggesting that in these cells Cav-1 positively regulates γ-secretase activity. In conclusion, EtOH differentially regulates γ-secretase activity in arterial EC and SMC, being stimulatory and inhibitory, respectively. These effects are both mediated by caveolin-1 inhibition which itself has opposite effects on γ-secretase in the two cell types. This mechanism may underlie, in part, the effects of moderate drinking on atherosclerosis.
MeSH term(s)	Humans ; Amyloid Precursor Protein Secretases/metabolism ; Caveolin 1/genetics ; Caveolin 1/metabolism ; Cells, Cultured ; Coronary Vessels/metabolism ; Endothelial Cells/metabolism ; Ethanol/pharmacology ; Myocytes, Smooth Muscle/metabolism ; RNA, Messenger/metabolism
Chemical Substances	Amyloid Precursor Protein Secretases (EC 3.4.-) ; Caveolin 1 ; Ethanol (3K9958V90M) ; RNA, Messenger ; CAV1 protein, human
Language	English
Publishing date	2023-01-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2724325-4
ISSN	2051-817X ; 2051-817X
ISSN (online)	2051-817X
ISSN	2051-817X
DOI	10.14814/phy2.15544
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Article: N-Glycans on the extracellular domain of the Notch1 receptor control Jagged-1 induced Notch signalling and myogenic differentiation of S100β resident vascular stem cells.

Corcoran, Eoin / Olayinka, Abidemi / di Luca, Mariana / Gusti, Yusof / Hakimjavadi, Roya / O'Connor, Brendan / Redmond, Eileen M / Cahill, Paul A

bioRxiv : the preprint server for biology

2023

Abstract: Notch signalling, critical for development and postnatal homeostasis of the vascular system, is highly regulated by several mechanisms including glycosylation. While the importance of O-linked glycosylation is widely accepted, the structure and function ... ...

Abstract	Notch signalling, critical for development and postnatal homeostasis of the vascular system, is highly regulated by several mechanisms including glycosylation. While the importance of O-linked glycosylation is widely accepted, the structure and function of N-glycans has yet to be defined. Here, we take advantage of lectin binding assays in combination with pharmacological, molecular, and site-directed mutagenetic approaches to study N-glycosylation of the Notch1 receptor. We find that several key oligosaccharides containing bisecting or core fucosylated structures decorate the receptor, control expression and receptor trafficking, and dictate Jagged-1 activation of Notch target genes and myogenic differentiation of multipotent S100β vascular stem cells. N-glycans at asparagine (N) 1241 and 1587 protect the receptor from accelerated degradation, while the oligosaccharide at N888 directly affects signal transduction. Conversely, N-linked glycans at N959, N1179, N1489 do not impact canonical signalling but inhibit differentiation. Our work highlights a novel functional role for N-glycans in controlling Notch1 signalling and differentiation of vascular stem cells.
Language	English
Publishing date	2023-12-06
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.11.17.567576
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Article ; Online: Vascular endothelium - Gatekeeper of vessel health.

Cahill, Paul A / Redmond, Eileen M

Atherosclerosis

2016 Volume 248, Page(s) 97–109

Abstract: The vascular endothelium is an interface between the blood stream and the vessel wall. Changes in this single cell layer of the artery wall are believed of primary importance in the pathogenesis of vascular disease/atherosclerosis. The endothelium ... ...

Abstract	The vascular endothelium is an interface between the blood stream and the vessel wall. Changes in this single cell layer of the artery wall are believed of primary importance in the pathogenesis of vascular disease/atherosclerosis. The endothelium responds to humoral, neural and especially hemodynamic stimuli and regulates platelet function, inflammatory responses, vascular smooth muscle cell growth and migration, in addition to modulating vascular tone by synthesizing and releasing vasoactive substances. Compromised endothelial function contributes to the pathogenesis of cardiovascular disease; endothelial 'dysfunction' is associated with risk factors, correlates with disease progression, and predicts cardiovascular events. Therapies for atherosclerosis have been developed, therefore, that are directed towards improving endothelial function.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/therapeutic use ; Atherosclerosis/physiopathology ; Cardiovascular Diseases/physiopathology ; Coronary Artery Disease/physiopathology ; Endothelium, Vascular/physiology ; Endothelium, Vascular/physiopathology ; Exercise ; Fibrinolytic Agents/therapeutic use ; Glycocalyx/chemistry ; Hemodynamics ; Humans ; Inflammation ; Mice ; Muscle, Smooth, Vascular/physiopathology ; Permeability ; Risk Factors ; Stem Cells/cytology ; Stress, Mechanical ; Vasoconstrictor Agents/therapeutic use ; Vasodilator Agents/therapeutic use
Chemical Substances	Anti-Inflammatory Agents ; Fibrinolytic Agents ; Vasoconstrictor Agents ; Vasodilator Agents
Language	English
Publishing date	2016-03-09
Publishing country	Ireland
Document type	Journal Article ; Review
ZDB-ID	80061-2
ISSN	1879-1484 ; 0021-9150
ISSN (online)	1879-1484
ISSN	0021-9150
DOI	10.1016/j.atherosclerosis.2016.03.007
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Article ; Online: Moderate dose alcohol protects against serum amyloid protein A1-induced endothelial dysfunction via both notch-dependent and notch-independent pathways.

Rajendran, Naresh K / Liu, Weimin / Chu, Charles C / Cahill, Paul A / Redmond, Eileen M

Alcoholism, clinical and experimental research

2021 Volume 45, Issue 11, Page(s) 2217–2230

Abstract: Background: Arterial endothelium plays a critical role in maintaining vessel homeostasis and preventing atherosclerotic cardiovascular disease (CVD). Low-to-moderate alcohol (EtOH) consumption is associated with reduced atherosclerosis and stimulates ... ...

Abstract	Background: Arterial endothelium plays a critical role in maintaining vessel homeostasis and preventing atherosclerotic cardiovascular disease (CVD). Low-to-moderate alcohol (EtOH) consumption is associated with reduced atherosclerosis and stimulates Notch signaling in endothelial cells. The aim of this study was to determine whether EtOH protects the endothelium against serum amyloid A1 (SAA1)-induced activation/injury, and to determine whether this protection is exclusively Notch-dependent. Methods and results: Human coronary artery endothelial cells (HCAEC) were stimulated or not with "pro-atherogenic" SAA1 (1 μM) in the absence or presence of EtOH (25 mM), the Notch ligand DLL4 (3 μg/ml), or the Notch inhibitor DAPT (20 μM). EtOH stimulated Notch signaling in HCAEC, as evidenced by increased expression of the Notch receptor and hrt target genes. Treatment with EtOH alone or stimulation of Notch signaling by DLL4 increased eNOS activity and enhanced HCAEC barrier function as assessed by trans-endothelial electrical resistance. Moreover, EtOH and DLL4 both inhibited SAA1-induced monolayer leakiness, cell adhesion molecule (ICAM, VCAM) expression, and monocyte adhesion. The effects of EtOH were Notch-dependent, as they were blocked with DAPT and by Notch receptor (N1, N4) knockdown. In contrast, EtOH's inhibition of SAA1-induced inflammatory cytokines (IL-6, IFN-γ) and reactive oxygen species (ROS) was Notch-independent, as these effects were unaffected by DAPT or by N1 and/or N4 knockdown. Conclusions: EtOH at moderate levels protects against SAA1-induced endothelial activation via both Notch-dependent and Notch-independent mechanisms. EtOH's maintenance of endothelium in a nonactivated state would be expected to preserve vessel homeostasis and protect against atherosclerosis development.
MeSH term(s)	Amyloidogenic Proteins/metabolism ; Cell Movement/drug effects ; Coronary Vessels/drug effects ; Coronary Vessels/metabolism ; Dose-Response Relationship, Drug ; Endothelial Cells/drug effects ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/metabolism ; Ethanol/pharmacology ; Humans ; Protective Agents ; Receptor, Notch1/metabolism ; Receptors, Notch/metabolism
Chemical Substances	Amyloidogenic Proteins ; Protective Agents ; Receptor, Notch1 ; Receptors, Notch ; Ethanol (3K9958V90M)
Language	English
Publishing date	2021-09-29
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	428999-7
ISSN	1530-0277 ; 0145-6008
ISSN (online)	1530-0277
ISSN	0145-6008
DOI	10.1111/acer.14706
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Article: Exosomal Composition, Biogenesis and Profiling Using Point-of-Care Diagnostics-Implications for Cardiovascular Disease.

Burtenshaw, Denise / Regan, Brian / Owen, Kathryn / Collins, David / McEneaney, David / Megson, Ian L / Redmond, Eileen M / Cahill, Paul Aidan

Frontiers in cell and developmental biology

2022 Volume 10, Page(s) 853451

Abstract: Arteriosclerosis is an important age-dependent disease that encompasses atherosclerosis, in-stent restenosis (ISR), pulmonary hypertension, autologous bypass grafting and transplant arteriosclerosis. Endothelial dysfunction and the proliferation of ... ...

Abstract	Arteriosclerosis is an important age-dependent disease that encompasses atherosclerosis, in-stent restenosis (ISR), pulmonary hypertension, autologous bypass grafting and transplant arteriosclerosis. Endothelial dysfunction and the proliferation of vascular smooth muscle cell (vSMC)-like cells is a critical event in the pathology of arteriosclerotic disease leading to intimal-medial thickening (IMT), lipid retention and vessel remodelling. An important aspect in guiding clinical decision-making is the detection of biomarkers of subclinical arteriosclerosis and early cardiovascular risk. Crucially, relevant biomarkers need to be good indicators of injury which change in their circulating concentrations or structure, signalling functional disturbances. Extracellular vesicles (EVs) are nanosized membraneous vesicles secreted by cells that contain numerous bioactive molecules and act as a means of intercellular communication between different cell populations to maintain tissue homeostasis, gene regulation in recipient cells and the adaptive response to stress. This review will focus on the emerging field of EV research in cardiovascular disease (CVD) and discuss how key EV signatures in liquid biopsies may act as early pathological indicators of adaptive lesion formation and arteriosclerotic disease progression. EV profiling has the potential to provide important clinical information to complement current cardiovascular diagnostic platforms that indicate or predict myocardial injury. Finally, the development of fitting devices to enable rapid and/or high-throughput exosomal analysis that require adapted processing procedures will be evaluated.
Language	English
Publishing date	2022-06-01
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2022.853451
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Article ; Online: Exosomal Composition, Biogenesis and Profiling Using Point-of-Care Diagnostics—Implications for Cardiovascular Disease

Denise Burtenshaw / Brian Regan / Kathryn Owen / David Collins / David McEneaney / Ian L. Megson / Eileen M. Redmond / Paul Aidan Cahill

Frontiers in Cell and Developmental Biology, Vol

2022 Volume 10

Abstract	Arteriosclerosis is an important age-dependent disease that encompasses atherosclerosis, in-stent restenosis (ISR), pulmonary hypertension, autologous bypass grafting and transplant arteriosclerosis. Endothelial dysfunction and the proliferation of vascular smooth muscle cell (vSMC)-like cells is a critical event in the pathology of arteriosclerotic disease leading to intimal-medial thickening (IMT), lipid retention and vessel remodelling. An important aspect in guiding clinical decision-making is the detection of biomarkers of subclinical arteriosclerosis and early cardiovascular risk. Crucially, relevant biomarkers need to be good indicators of injury which change in their circulating concentrations or structure, signalling functional disturbances. Extracellular vesicles (EVs) are nanosized membraneous vesicles secreted by cells that contain numerous bioactive molecules and act as a means of intercellular communication between different cell populations to maintain tissue homeostasis, gene regulation in recipient cells and the adaptive response to stress. This review will focus on the emerging field of EV research in cardiovascular disease (CVD) and discuss how key EV signatures in liquid biopsies may act as early pathological indicators of adaptive lesion formation and arteriosclerotic disease progression. EV profiling has the potential to provide important clinical information to complement current cardiovascular diagnostic platforms that indicate or predict myocardial injury. Finally, the development of fitting devices to enable rapid and/or high-throughput exosomal analysis that require adapted processing procedures will be evaluated.
Keywords	exosome (vesicle) ; atheroscelorsis ; stem cell repair mechanisms ; endothelial (dys)function ; point of care diagnosis ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2022-06-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
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Article: Reactive Oxygen Species (ROS), Intimal Thickening, and Subclinical Atherosclerotic Disease.

Burtenshaw, Denise / Kitching, Michael / Redmond, Eileen M / Megson, Ian L / Cahill, Paul A

Frontiers in cardiovascular medicine

2019 Volume 6, Page(s) 89

Abstract: Arteriosclerosis causes significant morbidity and mortality worldwide. Central to this process is the development of subclinical non-atherosclerotic intimal lesions before the appearance of pathologic intimal thickening and advanced atherosclerotic ... ...

Abstract	Arteriosclerosis causes significant morbidity and mortality worldwide. Central to this process is the development of subclinical non-atherosclerotic intimal lesions before the appearance of pathologic intimal thickening and advanced atherosclerotic plaques. Intimal thickening is associated with several risk factors, including oxidative stress due to reactive oxygen species (ROS), inflammatory cytokines and lipid. The main ROS producing systems
Language	English
Publishing date	2019-08-02
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2781496-8
ISSN	2297-055X
ISSN	2297-055X
DOI	10.3389/fcvm.2019.00089
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Article: Nox, Reactive Oxygen Species and Regulation of Vascular Cell Fate.

Burtenshaw, Denise / Hakimjavadi, Roya / Redmond, Eileen M / Cahill, Paul A

Antioxidants (Basel, Switzerland)

2017 Volume 6, Issue 4

Abstract: The generation of reactive oxygen species (ROS) and an imbalance of antioxidant defence mechanisms can result in oxidative stress. Several pro-atherogenic stimuli that promote intimal-medial thickening (IMT) and early arteriosclerotic disease progression ...

Abstract	The generation of reactive oxygen species (ROS) and an imbalance of antioxidant defence mechanisms can result in oxidative stress. Several pro-atherogenic stimuli that promote intimal-medial thickening (IMT) and early arteriosclerotic disease progression share oxidative stress as a common regulatory pathway dictating vascular cell fate. The major source of ROS generated within the vascular system is the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family of enzymes (Nox), of which seven members have been characterized. The Nox family are critical determinants of the redox state within the vessel wall that dictate, in part the pathophysiology of several vascular phenotypes. This review highlights the putative role of ROS in controlling vascular fate by promoting endothelial dysfunction, altering vascular smooth muscle phenotype and dictating resident vascular stem cell fate, all of which contribute to intimal medial thickening and vascular disease progression.
Language	English
Publishing date	2017-11-14
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox6040090
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Article ; Online: The NOX-ROS connection: targeting Nox1 control of N-cadherin shedding in vascular smooth muscle cells.

Redmond, Eileen M / Cahill, Paul A

Cardiovascular research

2012 Volume 93, Issue 3, Page(s) 386–387

MeSH term(s)	Animals ; Cadherins/metabolism ; Cell Movement/physiology ; ErbB Receptors/metabolism ; Muscle, Smooth, Vascular/cytology ; Muscle, Smooth, Vascular/enzymology ; NADH, NADPH Oxidoreductases/metabolism ; NADPH Oxidase 1
Chemical Substances	Cadherins ; Cdh2 protein, mouse ; NADH, NADPH Oxidoreductases (EC 1.6.-) ; NADPH Oxidase 1 (EC 1.6.3.-) ; NOX1 protein, mouse (EC 1.6.3.-) ; EGFR protein, mouse (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1)
Language	English
Publishing date	2012-01-20
Publishing country	England
Document type	Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvs020
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