Browsing
     by title


0-9 A B C D E F G H I J K L M N O P Q R S T U V W X Y Z

or enter first few letters:   
OK
See detailEndosymbiont-bearing trypanosomatids: kinetoplast ultrastructural characterization
Cavalcanti, DP; Thiry, Marc ULiege; De Souza, W et al

Poster (2001)

Detailed reference viewed: 4 (0 ULiège)
Full Text
Peer Reviewed
See detailEndothelial Cell Intracellular Ca2+ Concentration Is Increased Upon Breast Tumor Cell Contact and Mediates Tumor Cell Transendothelial Migration
Lewalle, J. M.; Cataldo, Didier ULiege; Bajou, Khalid ULiege et al

in Clinical & Experimental Metastasis (1998), 16(1), 21-9

Tumor cell extravasation is a determinant step in the process of hematogenous metastasis. The signal transduction pathways involved in the interactions between tumor cells and the vascular endothelium ... [more ▼]

Tumor cell extravasation is a determinant step in the process of hematogenous metastasis. The signal transduction pathways involved in the interactions between tumor cells and the vascular endothelium during transendothelial migration are still undefined. In the present study, we have investigated the influence of human breast adenocarcinoma cells (MCF7) on human umbilical vein endothelial cell (HUVEC) intracellular Ca2+ concentration ([Ca2+]i). We show that the contact between MCF7 cells and a confluent HUVEC monolayer induces an immediate and transient increase in HUVEC [Ca2+]i. This [Ca2+]i rise could not be elicited by tumor cell-conditioned medium, isolated tumor cell membranes, inert beads or normal breast epithelial cells, demonstrating the involvement of specific recognition mechanisms between MCF7 cells and HUVEC. Depletion of HUVEC intracellular Ca2+ stores by the endoplasmic reticulum Ca2+-ATPase inhibitor thapsigargin as well as the selective depletion of inositol 1,4,5-triphosphate (IP3)-sensitive Ca2+ stores by prior activation of HUVEC using histamine resulted in a complete inhibition of tumor cell-induced [Ca2+]i elevation. Similar results were obtained when HUVEC monolayers were treated with the tyrosine kinase inhibitor herbimycin A, suggesting a role for tyrosine kinase-associated cell surface receptors in tumor cell-endothelial cell interactions. The depletion of HUVEC intracellular Ca2+ stores by thapsigargin was also shown to delay MCF7-induced endothelial cell disjunction, to prevent their spreading on the subendothelial extracellular matrix and transendothelial migration in vitro. These results suggest that transient changes in endothelial [Ca2+]i may govern multiple steps of tumor cell extravasation. [less ▲]

Detailed reference viewed: 38 (7 ULiège)
Full Text
Peer Reviewed
See detailEndothelial cell-driven regulation of CD9 or motility-related protein-1 expression in multiple myeloma cells within the murine 5T33MM model and myeloma patients.
De Bruyne, Elke; Andersen, T. L.; De Raeve, Hendrik et al

in Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K (2006), 20(10), 1870-9

Detailed reference viewed: 19 (2 ULiège)
Full Text
Peer Reviewed
See detailEndothelial cells suppress monocyte activation through secretion of extracellular vesicles containing antiinflammatory microRNAs.
Njock, Makon-Sébastien ULiege; Cheng, Henry S.; Dang, Lan T. et al

in Blood (2015), 125(20), 3202-12

The blood contains high concentrations of circulating extracellular vesicles (EVs), and their levels and contents are altered in several disease states, including cardiovascular disease. However, the ... [more ▼]

The blood contains high concentrations of circulating extracellular vesicles (EVs), and their levels and contents are altered in several disease states, including cardiovascular disease. However, the function of circulating EVs, especially the microRNAs (miRNAs) that they contain, are poorly understood. We sought to determine the effect of secreted vesicles produced by quiescent endothelial cells (ECs) on monocyte inflammatory responses and to assess whether transfer of microRNAs occurs between these cells. We observed that monocytic cells cocultured (but not in contact) with ECs were refractory to inflammatory activation. Further characterization revealed that endothelium-derived EVs (EC-EVs) suppressed monocyte activation by enhancing immunomodulatory responses and diminishing proinflammatory responses. EVs isolated from mouse plasma also suppressed monocyte activation. Importantly, injection of EC-EVs in vivo repressed monocyte/macrophage activation, confirming our in vitro findings. We found that several antiinflammatory microRNAs were elevated in EC-EV-treated monocytes. In particular, miR-10a was transferred to monocytic cells from EC-EVs and could repress inflammatory signaling through the targeting of several components of the NF-kappaB pathway, including IRAK4. Our findings reveal that ECs secrete EVs that can modulate monocyte activation and suggest that altered EV secretion and/or microRNA content may affect vascular inflammation in the setting of cardiovascular disease. [less ▲]

Detailed reference viewed: 15 (0 ULiège)
Full Text
Peer Reviewed
See detailEndothelial exosomes contribute to the antitumor response during breast cancer neoadjuvant chemotherapy via microRNA transfer.
Bovy, Nicolas ULiege; Blomme, Benoît ULiege; Freres, Pierre ULiege et al

in Oncotarget (2015)

The interaction between tumor cells and their microenvironment is an essential aspect of tumor development. Therefore, understanding how this microenvironment communicates with tumor cells is crucial for ... [more ▼]

The interaction between tumor cells and their microenvironment is an essential aspect of tumor development. Therefore, understanding how this microenvironment communicates with tumor cells is crucial for the development of new anti-cancer therapies. MicroRNAs (miRNAs) are small non-coding RNAs that inhibit gene expression. They are secreted into the extracellular medium in vesicles called exosomes, which allow communication between cells via the transfer of their cargo. Consequently, we hypothesized that circulating endothelial miRNAs could be transferred to tumor cells and modify their phenotype. Using exogenous miRNA, we demonstrated that endothelial cells can transfer miRNA to tumor cells via exosomes. Using miRNA profiling, we identified miR-503, which exhibited downregulated levels in exosomes released from endothelial cells cultured under tumoral conditions. The modulation of miR-503 in breast cancer cells altered their proliferative and invasive capacities. We then identified two targets of miR-503, CCND2 and CCND3. Moreover, we measured increased plasmatic miR-503 in breast cancer patients after neoadjuvant chemotherapy, which could be partly due to increased miRNA secretion by endothelial cells. Taken together, our data are the first to reveal the involvement of the endothelium in the modulation of tumor development via the secretion of circulating miR-503 in response to chemotherapy treatment. [less ▲]

Detailed reference viewed: 285 (55 ULiège)
Full Text
Peer Reviewed
See detailEndothelial LGALS9 splice variant expression in endothelial cell biology and angiogenesis
Heusschen, Roy ULiege; Schulkens, Iris; van Beijnum, Judy et al

in Biochimica et Biophysica Acta - Molecular Basis of Disease (2014), 1842(2), 284-92

Detailed reference viewed: 19 (6 ULiège)
Full Text
Peer Reviewed
See detailEndothelial miRNAs as Cellular Messengers in Cardiometabolic Diseases.
Njock, Makon-Sébastien ULiege; Fish, Jason E.

in Trends in endocrinology and metabolism: TEM (2017), 28(3), 237-246

Metabolic syndrome is a clustering of risk factors that increases susceptibility to serious cardiometabolic complications, including type 2 diabetes (T2D) and myocardial infarction. Understanding the ... [more ▼]

Metabolic syndrome is a clustering of risk factors that increases susceptibility to serious cardiometabolic complications, including type 2 diabetes (T2D) and myocardial infarction. Understanding the underlying mechanisms will advance the development of diagnostic and therapeutic approaches. A prominent feature of cardiometabolic diseases is endothelial dysfunction. Endothelial cell (EC) homeostasis and response to pathological stimuli are controlled by gene regulatory networks in which miRNAs play a critical role. Recently, miRNAs have been implicated as cell-cell messengers that can influence cellular function. This review investigates the known and potential roles for miRNA-based cell-cell communication in the control of cardiovascular health and explores the value of identifying miRNA biomarkers and developing therapeutics that harness or antagonize miRNA-based communication. [less ▲]

Detailed reference viewed: 16 (0 ULiège)
Full Text
Peer Reviewed
See detailEndothelial SHIP2 suppresses Nox2 NADPH oxidase-dependent vascular oxidative stress, endothelial dysfunction and systemic insulin resistance
Watt, NT; Gage, MC; Patel, PA et al

in Diabetes (2017), 66(11), 2808-2821

Shc homology 2-containing inositol 5´ phosphatase-2 (SHIP2) is as lipid phosphatase which inhibits insulin signaling downstream of phosphoinositide-3-kinase (PI3K); its role in vascular function is poorly ... [more ▼]

Shc homology 2-containing inositol 5´ phosphatase-2 (SHIP2) is as lipid phosphatase which inhibits insulin signaling downstream of phosphoinositide-3-kinase (PI3K); its role in vascular function is poorly understood. To examine its role in endothelial cell (EC) biology, we generated mice with catalytic inactivation of one SHIP2 allele selectively in EC (ECSHIP2Δ/+). Hyperinsulinemic euglycemic clamping studies revealed ECSHIP2Δ/+ were resistant to insulin-stimulated glucose uptake in adipose tissue and skeletal muscle, compared with littermate controls. EC from ECSHIP2Δ/+ had increased basal expression and activation of PI3K downstream targets, including Akt and endothelial nitric oxide synthase (eNOS), although incremental activation by insulin and shear stress was impaired. Insulin-mediated vasodilation was blunted in ECSHIP2Δ/+, as was aortic nitric oxide bioavailability. Acetylcholine-induced vasodilation was also impaired in ECSHIP2Δ/+, which was exaggerated in the presence of a superoxide dismutase/catalase mimetic. Superoxide abundance was elevated in ECSHIP2Δ/+ EC, and was suppressed by PI3K and Nox2 NADPH oxidase inhibitors. These findings were phenocopied in healthy human EC after SHIP2 silencing. Our data suggest that endothelial SHIP2 is required to maintain normal systemic glucose homeostasis and prevent oxidative stress-induced endothelial dysfunction. [less ▲]

Detailed reference viewed: 28 (2 ULiège)
Full Text
Peer Reviewed
See detailEndothelial-derived microparticles: Biological conveyors at the crossroad of inflammation, thrombosis and angiogenesis
Leroyer, Aurélie S.; Anfosso, Francine; Lacroix, Romaric et al

in Thrombosis and Haemostasis (2010), 104(3), 456-63

Endothelial microparticles (EMP) are complex vesicular structures that can be shed by activated or apoptotic endothelial cells. EMP are composed of a phospholipid bilayer that exposes transmembrane ... [more ▼]

Endothelial microparticles (EMP) are complex vesicular structures that can be shed by activated or apoptotic endothelial cells. EMP are composed of a phospholipid bilayer that exposes transmembrane proteins and receptors and encloses cytosolic components such as enzymes, transcription factors and mRNA derived from their parent cells. Thus, EMP behave as biological conveyors playing a key role in the tuning of vascular homeostasis. This review focuses on the multifaceted roles of EMP, notably in coagulation, inflammation and angiogenesis and also on the mechanisms that trigger their formation. In this context, EMP could compromise vascular homeostasis and then represent key players in the pathogenesis of several inflammatory and thrombotic diseases. Consequently, elucidating their role and their mechanisms of formation will bring new insights into the understanding of endothelial-associated diseases. Moreover, in the future, it can open novel therapeutic perspectives based on the inhibition of EMP release. [less ▲]

Detailed reference viewed: 29 (0 ULiège)
Full Text
Peer Reviewed
See detailEndothelin in the equine hypoxic pulmonary vasoconstrictive response to acute hypoxia
Benamou, A. E.; Marlin, D. J.; Lekeux, Pierre ULiege

in Equine Veterinary Journal (2001), 33(4), 345-353

Elevated concentrations of endothelin (ET), a potent endothelium-derived vasoactive peptide, have been reported in a number of pathophysiological conditions associated with pulmonary hypertension, both in ... [more ▼]

Elevated concentrations of endothelin (ET), a potent endothelium-derived vasoactive peptide, have been reported in a number of pathophysiological conditions associated with pulmonary hypertension, both in the horse and other species. We have previously shown, both in vitro and in vivo, that the pulmonary and systemic vascular response to exogenous ET is mediated predominantly via ET(A) receptors. Our hypothesis in the present study was that ET is involved in the equine hypoxic pulmonary vasoconstrictive response to acute hypoxia. In this study, we investigated the effects of a selective ET(A) receptor antagonist on hypoxic pulmonary hypertension in the mature horse. Horses were exposed to a 10 min period of hypoxia (F(I)O2 approximately 0.11) on 2 occasions, with and without pretreatment with the selective ET(A) receptor antagonist TBC11251 (10 mg/kg bwt i.v.). Hypoxia increased mean pulmonary artery pressure (PAP) from 18.3+/-0.9 (mean +/- s.e. normoxia) to 28.0+/-0.8 mmHg (hypoxia) in the session without ET(A) receptor antagonism. Carotid arterial pressure (CAP) also increased progressively throughout the period of hypoxic challenge and at the end was 153+/-5 mmHg (hypoxia) compared to during normoxia (140+/-5 mmHg). There was no significant overall effect of ET(A) receptor antagonism on the haemodynamic or ventilatory responses to acute hypoxia. However, between 5 and 10 min of hypoxia there was a trend for the mean PAP to diverge in the 2 treatments, which just failed to reach significance at 10 min of hypoxia (P = 0.053). In conclusion, this study describes the haemodynamic and ventilatory changes in response to a period of acute hypoxia in the adult horse. The results do not support a role for ET as a mediator of acute HPV in the horse, but suggest that it may be involved as a modulator or in the slower (>10 min) phase of HPV. [less ▲]

Detailed reference viewed: 25 (1 ULiège)
Peer Reviewed
See detailEndothelin-1 as a serum biomarker in idiopathic pulmonary fibrosis in dogs
Krafft, Emilie ULiege; Heikkilä, H.P.; Jespers, P. et al

in Proceedings of the 20th ECVIM-CA Congress (2010)

Detailed reference viewed: 10 (1 ULiège)
Full Text
Peer Reviewed
See detailEndothelin-1 is a critical mediator of myogenic tone in tumor arterioles: implications for cancer treatment.
Sonveaux, Pierre; Dessy; MARTINIVE, Philippe ULiege et al

in Cancer Research (2004), 1(64), 3209-14

Although derived from the host tissue, the tumor vasculature is under the influence of the tumor microenvironment and needs to adapt to the resistance to blood flow inherent to the dynamics of tumor ... [more ▼]

Although derived from the host tissue, the tumor vasculature is under the influence of the tumor microenvironment and needs to adapt to the resistance to blood flow inherent to the dynamics of tumor growth. Such vascular remodeling can offer selective targets to pharmacologically modulate tumor perfusion and thereby improve the efficacy of conventional anticancer treatments. Radiotherapy and chemotherapy can, indeed, take advantage of a better tumor oxygenation and drug delivery, respectively, both partly dependent on the tumor blood supply. Here, we showed that isolated tumor arterioles mounted in a pressure myograph have the ability, contrary to size-matched healthy arterioles, to contract in response to a transluminal pressure increase. This myogenic tone was exquisitely dependent on the endothelin-1 pathway because it was completely abolished by the selective endothelin receptor A (ETA) antagonist BQ123. This selectivity was additionally supported by the large increase in endothelin-1 abundance in tumors and the higher density of the ETA receptors in tumor vessels. We also documented by using laser Doppler microprobes and imaging that administration of the ETA antagonist led to a significant increase in tumor blood flow, whereas the perfusion in control healthy tissue was not altered. Finally, we provided evidence that acute administration of the ETA antagonist could significantly stimulate tumor oxygenation, as determined by electron paramagnetic resonance oximetry, and increase the efficacy of low-dose, clinically relevant fractionated radiotherapy. Thus, blocking the tumor-selective increase in the vascular endothelin-1/ETA pathway led us to unravel an important reserve of vasorelaxation that can be exploited to selectively increase tumor response to radiotherapy. [less ▲]

Detailed reference viewed: 67 (9 ULiège)
Peer Reviewed
See detailEndothelium in aneurysmal bone cyst.
Aho, H. J.; Aho, A. J.; Pelliniemi, L. J. et al

in Histopathology (1985), 9(4), 381-7

The surface of the large cystic spaces and dilated blood vessels in seven cases of aneurysmal bone cysts was studied. The endothelium of the blood vessels was surrounded by a layer of collagen types IV ... [more ▼]

The surface of the large cystic spaces and dilated blood vessels in seven cases of aneurysmal bone cysts was studied. The endothelium of the blood vessels was surrounded by a layer of collagen types IV and V, and the endothelial cells contained factor VIII related antigen demonstrated by the peroxidase anti-peroxidase technique. Some blood vessels were dilated resembling small aneurysmal spaces. The visible surfaces of the aneurysmal spaces were devoid of collagen types IV and V, and of factor VIII related antigen. Ultrastructural analysis of paraffin embedded sections did not show the characteristic fine structural features of endothelium covering the aneurysmal spaces. It is concluded that the large spaces in aneurysmal bone cysts are devoid of basement membranes and endothelial cells. The absence of endothelium may explain the abundance of haemorrhages in these lesions. Immunocytochemical demonstration of endothelial antigen provides a valuable tool for the differential diagnosis between aneurysmal bone cysts and vascular tumours. [less ▲]

Detailed reference viewed: 5 (0 ULiège)
Full Text
Peer Reviewed
See detailEndothelium-Dependent Effects of Heat Shock on Vasomotor Tone: Role of eNOS and HSP70
Salomone, Salvatore; Plumier, Jean-Christophe ULiege

in Carrasco, Joao; Mota, Matheus (Eds.) Endothelium and Epithelium: Composition, Functions and Pathology (2011)

Detailed reference viewed: 37 (1 ULiège)
Peer Reviewed
See detailEndothelium-specific expression of the microRNA miR-146a by using the RCAS system
Fontaine, Marie ULiege; Halkein, Julie; Tabruyn, Sébastien et al

Poster (2013, May 17)

Detailed reference viewed: 14 (3 ULiège)
Full Text
Peer Reviewed
See detailL'endotoxémie dans l'espèce équine. 1ère partie: étiologie et physiopathologie.
Amory, Hélène ULiege

in Pratique Vétérinaire Equine (1996), 28

Detailed reference viewed: 46 (8 ULiège)
See detailEndotoxémie et diarrhée aiguë
Amory, Hélène ULiege

in Proceedings of the Annual meeting of the French Equine Veterinary Association (AVEF) (1996)

Detailed reference viewed: 20 (4 ULiège)
Full Text
See detailEndotoxin-induced alterations in renal oxygen consumption: an ESR oximetry study
Quoilin, Caroline ULiege; Grammenos, Angeliki ULiege; Gallez, Bernard et al

Poster (2011, August)

The kidney, one of the most injured organs in critically ill patients, is faced with unique challenges for molecular oxygen regulation. Recent research activities in the pathophysiological mechanism of ... [more ▼]

The kidney, one of the most injured organs in critically ill patients, is faced with unique challenges for molecular oxygen regulation. Recent research activities in the pathophysiological mechanism of acute renal injury (ARI) emphasize the central role of hemodynamic and inflammatory events in septic shock. More particularly, two mechanisms have been postulated to explain the inability of the injured kidney to extract oxygen: tissue hypoxia and cellular energetic metabolism dysfunction. The present investigation was carried out to characterize the effects of bacterial endotoxin on the oxygen consumption of human tubular proximal cell line (PTC) by using the very sensitive electron spin resonance oximetry method. Oxygen consumption was shown to decrease quite markedly in cells treated with lipopolysaccharide (LPS) from 16.52 ± 2.51 (n=6) in the control group to: 12.94 ± 2.62 (n=3) in the short incubation time group (6h) and 10.86 ± 2.20 (n=3) in the long incubation time group (18h). This decrease in oxygen consumption in renal cells after LPS challenge may be in relation with a metabolic down-regulation. Renal energetic are deranged in sepsis not just because O2 delivery is impaired but perhaps also because the ability of cells to utilize available O2 is compromised. [less ▲]

Detailed reference viewed: 57 (20 ULiège)
Full Text
Peer Reviewed
See detailEndotoxin-induced basal respiration alterations of renal HK-2 cells: A sign of pathologic metabolism down-regulation
Quoilin, Caroline ULiege; Mouithys-Mickalad, Ange ULiege; Duranteau, Jacques et al

in Biochemical and Biophysical Research Communications (2012), 423(2), 350-354

To study the mechanism of oxygen regulation in inflammation-induced acute kidney injury, we investigate the effects of a bacterial endotoxin (lipopolysaccharide, LPS) on the basal respiration of proximal ... [more ▼]

To study the mechanism of oxygen regulation in inflammation-induced acute kidney injury, we investigate the effects of a bacterial endotoxin (lipopolysaccharide, LPS) on the basal respiration of proximal tubular epithelial cells (HK-2) both by high-resolution respirometry and electron spin resonance spectroscopy. These two complementary methods have shown that HK-2 cells exhibit a decreased oxygen consumption rate when treated with LPS. Surprisingly, this cellular respiration alteration persists even after the stress factor was removed. We suggested that this irreversible decrease in renal oxygen consumption after LPS challenge is related to a pathologic metabolic down-regulation such as a lack of oxygen utilization by cells. [less ▲]

Detailed reference viewed: 37 (14 ULiège)