Effects of a thiol antioxidant on leucocyte adherence to aortic endothelium during atherogenesis: Quantitative SEM assessment

1993 ◽  
Vol 51 ◽  
pp. 792-793
Author(s):  
Keith A. Robinson ◽  
Russell M. Medford ◽  
R. Wayne Alexander
Keyword(s):  
Endothelial Cells ◽  
New Zealand ◽  
Pyrrolidine Dithiocarbamate ◽  
Fatty Streak ◽  
Ringer’S Solution ◽  
Thiol Antioxidant ◽  
Arterial Endothelial Cells ◽  
Attachment Process ◽  
Leucocyte Adherence

Dysfunction of arterial endothelial cells (EC) leading to adherence of circulating leucocytes (WBC) is a pivotal step in atherogenesis, preceding fatty streak formation. The attachment process is mediated at least in part by inducible endothelial-leucocyte adhesion molecules (ELAMs) on the EC surface which interact with WBC counterreceptors. Expression of VCAM-1, a monocyte selective adhesion molecule, by IL-1 and TNF stimulated vascular EC in vitro was shown to be inhibited by a thiol antioxidant (pyrrolidine dithiocarbamate, PDTC). In this study we analyzed the effect of PDTC administered to cholesterol-fed rabbits, on WBC attachment to lesion-prone sites of the aorta using SEM morphometry.New Zealand White (NZW) rabbits (2-3 kg) were fed 1% cholesterol for 3 d. The day before feeding, venous cannulas were introduced, and PDTC (20 mg/kg) or vehicle (0.1 M PBS) was given twice daily throughout. The animals were euthanatized at 4 d and the aortas pressure perfusion fixed with buffered 2.5% glutaraldehyde after rinse with Ringer‘s solution containing heparin (10 u/ml).

scholarly journals Venous and Arterial Endothelial Cells from Human Umbilical Cords: Potential Cell Sources for Cardiovascular Research

2021 ◽  
Vol 22 (2) ◽  
pp. 978
Author(s):  
Skadi Lau ◽  
Manfred Gossen ◽  
Andreas Lendlein ◽  
Friedrich Jung
Keyword(s):  
Endothelial Cells ◽  
Umbilical Cord ◽  
Membrane Integrity ◽  
Cell Types ◽  
Cell Number ◽  
Human Umbilical Cord ◽  
Cardiovascular Research ◽  
Cardiovascular Devices ◽  
Arterial Endothelial Cells

Although cardiovascular devices are mostly implanted in arteries or to replace arteries, in vitro studies on implant endothelialization are commonly performed with human umbilical cord-derived venous endothelial cells (HUVEC). In light of considerable differences, both morphologically and functionally, between arterial and venous endothelial cells, we here compare HUVEC and human umbilical cord-derived arterial endothelial cells (HUAEC) regarding their equivalence as an endothelial cell in vitro model for cardiovascular research. No differences were found in either for the tested parameters. The metabolic activity and lactate dehydrogenase, an indicator for the membrane integrity, slightly decreased over seven days of cultivation upon normalization to the cell number. The amount of secreted nitrite and nitrate, as well as prostacyclin per cell, also decreased slightly over time. Thromboxane B2 was secreted in constant amounts per cell at all time points. The Von Willebrand factor remained mainly intracellularly up to seven days of cultivation. In contrast, collagen and laminin were secreted into the extracellular space with increasing cell density. Based on these results one might argue that both cell types are equally suited for cardiovascular research. However, future studies should investigate further cell functionalities, and whether arterial endothelial cells from implantation-relevant areas, such as coronary arteries in the heart, are superior to umbilical cord-derived endothelial cells.

Differences in secretion of prostacyclin by venous and arterial endothelial cells grown in vitro in a static versus a mechanically active environment

1989 ◽  
Vol 10 (3) ◽  
pp. 0292-0298 ◽  
Author(s):  
Gilbert R. Upchurch ◽  
Albert J. Banes ◽  
Willis H. Wagner ◽  
Fuad Ramadan ◽  
Garnett W. Link ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Arterial Endothelial Cells

Resveratrol attenuates TNF-α-induced activation of coronary arterial endothelial cells: role of NF-κB inhibition

2006 ◽  
Vol 291 (4) ◽  
pp. H1694-H1699 ◽  
Author(s):  
Anna Csiszar ◽  
Kira Smith ◽  
Nazar Labinskyy ◽  
Zsuzsanna Orosz ◽  
Aracelie Rivera ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Reporter Gene ◽  
Endothelial Activation ◽  
Bone Morphogenetic Protein 2 ◽  
Luciferase Expression ◽  
Pyrrolidine Dithiocarbamate ◽  
Tnf Α ◽  
Gene Assay ◽  
Cardioprotective Effects ◽  
Arterial Endothelial Cells

Epidemiological studies suggest that Mediterranean diets rich in resveratrol are associated with reduced risk of coronary artery disease. However, the mechanisms by which resveratrol exerts its cardioprotective effects are not completely understood. Because TNF-α-induced endothelial activation and vascular inflammation play a critical role in vascular aging and atherogenesis, we evaluated whether resveratrol inhibits TNF-α-induced signal transduction in human coronary arterial endothelial cells (HCAECs). We found that TNF-α significantly increased adhesiveness of the monocytic THP-1 cells to HCAECs, an effect that could be inhibited by pretreatment with resveratrol and the NF-κB inhibitor pyrrolidine dithiocarbamate. Previously, we found that TNF-α activates NAD(P)H oxidases, and our recent data showed that TNF-α-induced endothelial activation was prevented by the NAD(P)H oxidase inhibitor apocynin or catalase plus SOD. Resveratrol also inhibited H2O2-induced monocyte adhesiveness. Using a reporter gene assay, we found that, in HCAECs, TNF-α significantly increased NF-κB activity, which could be inhibited by resveratrol (>50% inhibition at 10−6 mol/l) and pyrrolidine dithiocarbamate. Resveratrol also inhibited TNF-α-induced, NF-κB-driven luciferase expression in rat aortas electroporated with the reporter gene construct. In TNF-α-treated HCAECs, resveratrol (in the submicromolar range) significantly attenuated expression of NF-κB-dependent inflammatory markers inducible nitric oxide synthase, IL-6, bone morphogenetic protein-2, ICAM-1, and VCAM. Thus resveratrol at nutritionally relevant concentrations inhibits TNF-α-induced NF-κB activation and inflammatory gene expression and attenuates monocyte adhesiveness to HCAECs. We propose that these anti-inflammatory actions of resveratrol are responsible, at least in part, for its cardioprotective effects.

Abstract 1636: Adverse Effect of Estrogen on Bone Morphogenetic Protein Receptor Signal Pathway in Pulmonary Arterial Endothelial Cells

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Hiroaki Ichimori ◽  
Shigetoyo Kogaki ◽  
Hidekazu Ishida ◽  
Jun Narita ◽  
Toshiki Uchikawa ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Estrogen Receptor ◽  
Bone Morphogenetic Protein ◽  
Signal Pathway ◽  
Bone Morphogenetic Protein Receptor ◽  
Protein Receptor ◽  
Morphogenetic Protein ◽  
Pulmonary Arterial ◽  
Arterial Endothelial Cells

Gender differences in the development of Pulmonary Artery Hypertension (PAH) have been documented in both human and animal studies. In human, idiopathic PAH is predominantly a disease of young women in their child-bearing years, which suggests a role of female sex hormones in the pathogenesis of PAH. However, the effect of sex hormones on pulmonary vasculatures and the development of PAH has not been fully understood. Recent researches have revealed genetic predisposition such as BMPR (Bone Morphogenetic Protein Receptor). The aim of the present study is to investigate the effect of β-estradiol (E2) and oxygen concentration upon BMPR signal pathway in pulmonary arterial endothelial cells (PAEC) in vitro. Human and rat PAEC were cultured and we examined the expression of BMPR2, BMP-regulated Smads, and Id1 under 21% or 1% O 2 with BMP2 stimulation. Then, we investigate changes in the expression of these molecules in the presence of E2 with or without estrogen receptor antagonist (ICI 182.780.). First, we confirmed that estrogen receptor α and β were expressed in both PAECs. Second, we demonstrated that the expression of mRNA transcripts for BMPR2 and Id1 in PAEC was reduced after exposure to 24 hours’ hypoxia. In addition, E2 decreased the expression of phosphorylated Smad (p-Smad)1/5/8 in a dose-dependent manner (10 −10 M-10 −7 M) and p-Smad1/5/8 expression were decreased about 80% by 10 −7 M of E2. These attenuation of p-Smad1/5/8 expression were rescued by ICI182.780. Third, under normoxic condition with cobalt chloride or deferoxamine to prevent the degradation of HIF (hypoxia-inducible factor)-1α, the presence of E2 decreased the expression of p-Smad1/5/8 like under hypoxia. Conversely, administration of HIF-1α inhibitor (YC-1) canceled the reduced expression of p-Smad1/5/8 like under normoxia. Under hypoxia, the presence of E2 attenuates the BMPR signal pathway in PAEC in vitro. Our data indicated that the advance effect of E2 on BMPR signal pathway was associated with HIF-1α and estrogen receptor. Our observations provide the first evidence that female sex hormone affects on BMPR signal pathway, which can offer new strategies for the treatment of PAH.

scholarly journals Differences in secretion of prostacyclin by venous and arterial endothelial cells grown in vitro in a static versus a mechanically active environment

1989 ◽  
Vol 10 (3) ◽  
pp. 292-298 ◽  
Author(s):  
Gilbert R. Upchurch ◽  
Albert J. Banes ◽  
Willis H. Wagner ◽  
Fuad Ramadan ◽  
Garnett W. Link ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Arterial Endothelial Cells

Stromal cells expressing ephrin-B2 promote the growth and sprouting of ephrin-B2+ endothelial cells

Blood ◽  
2001 ◽  
Vol 98 (4) ◽  
pp. 1028-1037 ◽  
Author(s):  
Xiu-Qin Zhang ◽  
Nobuyuki Takakura ◽  
Yuichi Oike ◽  
Tomohisa Inada ◽  
Nicholas W. Gale ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Stromal Cells ◽  
Network Formation ◽  
Smooth Muscle Actin ◽  
Cell System ◽  
Vascular Network ◽  
Functional Studies ◽  
Vasculogenesis And Angiogenesis ◽  
Arterial Endothelial Cells

Ephrin-B2 is a transmembrane ligand that is specifically expressed on arterial endothelial cells (ECs) and surrounding cells and interacts with multiple EphB class receptors. Conversely, EphB4, a specific receptor for ephrin-B2, is expressed on venous ECs, and both ephrin-B2 and EphB4 play essential roles in vascular development. The bidirectional signals between EphB4 and ephrin-B2 are thought to be specific for the interaction between arteries and veins and to regulate cell mixing and the making of particular boundaries. However, the molecular mechanism during vasculogenesis and angiogenesis remains unclear. Manipulative functional studies were performed on these proteins in an endothelial cell system. Using in vitro stromal cells (OP9 cells) and a paraaortic splanchnopleura (P-Sp) coculture system, these studies found that the stromal cells expressing ephrin-B2 promoted vascular network formation and ephrin-B2+ EC proliferation and that they also induced the recruitment and proliferation of α-smooth muscle actin (α-SMA)–positive cells. Stromal cells expressing EphB4 inhibited vascular network formation, ephrin-B2+ EC proliferation, and α-SMA+ cell recruitment and proliferation. Thus, these data suggest that ephrin-B2 and EphB4 mediate reciprocal interactions between arterial and venous ECs and surrounding cells to form each characteristic vessel.

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