Soluble vascular endothelial-cadherin and auto-antibodies to human vascular endothelial-cadherin in human diseases: Two new biomarkers of endothelial dysfunction

Blaise, S.; Polena, Helena; Vilgrain, Isabelle

doi:10.1177/1358863x15591201

Cited by 23 publications

(15 citation statements)

References 42 publications

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“…In addition, the cytoplasmic tail of VE-cadherin links to the cytoskeleton by binding directly and indirectly with various catenins, including β-catenin [8,15]. Targeting either the extracellular domain or the cytoplasmic tail deleteriously affects the junctional strength and leads to vascular permeability [16].…”

Section: Introductionmentioning

confidence: 99%

Exposure to Zinc Oxide Nanoparticles Disrupts Endothelial Tight and Adherens Junctions and Induces Pulmonary Inflammatory Cell Infiltration

Chen

et al. 2020

IJMS

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Zinc oxide nanoparticles (ZnONPs) are frequently encountered nanomaterials in our daily lives. Despite the benefits of ZnONPs in a variety of applications, many studies have shown potential health hazards of exposure to ZnONPs. We have shown that oropharyngeal aspiration of ZnONPs in mice increases lung inflammation. However, the detailed mechanisms underlying pulmonary inflammatory cell infiltration remain to be elucidated. Endothelium functions as a barrier between the blood stream and the blood vessel wall. Endothelial barrier dysfunction may increase infiltration of immune cells into the vessel wall and underlying tissues. This current study examined the effects of ZnONPs exposure on endothelial barriers. ZnONPs exposure increased leukocyte infiltration in the mouse lungs. In endothelial cells, ZnONPs reduced the continuity of tight junction proteins claudin-5 and zonula occludens-1 (ZO-1) at the cell junctions. ZnONPs induced adherens junction protein VE-cadherin internalization from membrane to cytosol and dissociation with β-catenin, leading to reduced and diffused staining of VE-cadherin and β-catenin at cell junctions. Our results demonstrated that ZnONPs disrupted both tight and adherens junctions, compromising the integrity and stability of the junction network, leading to inflammatory cell infiltration. Thus, ZnONPs exposure in many different settings should be carefully evaluated for vascular effects and subsequent health impacts.

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Section: Introductionmentioning

confidence: 99%

Exposure to Zinc Oxide Nanoparticles Disrupts Endothelial Tight and Adherens Junctions and Induces Pulmonary Inflammatory Cell Infiltration

Chen

et al. 2020

IJMS

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“…Cadherins are known to play an important role in vascular cell function and angiogenesis, while Wnt signaling has been implicated to promote vascular remodeling and even cardiovascular regeneration. 36,37 Using three different functional assays we confirmed that editing-induced targetome changes result in angiogenesis-associated functional changes. We assessed the effect of WT-microRNAs and ED-microRNAs on in vitro scratch-wound healing and tube formation, and ex vivo neovessel sprouting, and consistently found that ED-microRNAs had increased pro-angiogenic properties compared to the WT-microRNAs.…”

Section: Discussionmentioning

confidence: 59%

Adenosine-to-Inosine Editing of Vasoactive MicroRNAs Alters Their Targetome and Function in Ischemia

Kwast

Parma

Bent

et al. 2020

Molecular Therapy - Nucleic Acids

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Adenosine-to-inosine (A-to-I) editing in the seed sequence of microRNAs can shift the microRNAs’ targetomes and thus their function. Using public RNA-sequencing data, we identified 35 vasoactive microRNAs that are A-to-I edited. We quantified A-to-I editing of the primary (pri-)microRNAs in vascular fibroblasts and endothelial cells. Nine pri-microRNAs were indeed edited, and editing consistently increased under ischemia. We determined mature microRNA editing for the highest expressed microRNAs, i.e., miR-376a-3p, miR-376c-3p, miR-381-3p, and miR-411-5p. All four mature microRNAs were edited in their seed sequence. We show that both ADAR1 and ADAR2 (adenosine deaminase acting on RNA 1 and RNA 2) can edit pri-microRNAs in a microRNA-specific manner. MicroRNA editing also increased under ischemia in vivo in a murine hindlimb ischemia model and ex vivo in human veins. For each edited microRNA, we confirmed a shift in targetome. Expression of the edited microRNA targetomes, not the wild-type targetomes, was downregulated under ischemia in vivo . Furthermore, microRNA editing enhanced angiogenesis in vitro and ex vivo . In conclusion, we show that microRNA A-to-I editing is a widespread phenomenon, induced by ischemia. Each editing event results in a novel microRNA with a unique targetome, leading to increased angiogenesis.

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“…We have previously shown that TLR2 activation by LTA from Staphylococcus aureus has deleterious effects on endothelial cell adhesion and increases permeability ( 19 ). Cadherin is critical in maintaining the integrity of intercellular junctions creating a restrictive endothelial barrier ( 20 ). Soluble vascular endothelial cadherin has been shown to be a prognostic marker in inflammatory disease states ( 20 , 21 ).…”

Section: Discussionmentioning

confidence: 99%

“…Cadherin is critical in maintaining the integrity of intercellular junctions creating a restrictive endothelial barrier ( 20 ). Soluble vascular endothelial cadherin has been shown to be a prognostic marker in inflammatory disease states ( 20 , 21 ). We found the mean of measured plasma markers of inflammation (IL-6, hepcidin) and endothelial barrier dysfunction (sVE cadherin) to be much higher than values reported for healthy subjects ( 14 , 15 , 22 ).…”

Section: Discussionmentioning

confidence: 99%

Quantification of Lipoteichoic Acid in Hemodialysis Patients With Central Venous Catheters

Pai¹,

Garba²,

Neumann³

et al. 2018

Front. Med.

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Hemodialysis patients with central venous catheters (CVCs) have chronic systemic inflammation, the source of which may be related to intraluminal bacterial biofilm. There is currently no non-invasive method to adequately evaluate intraluminal biofilm. Lipoteichoic acid (LTA) is a Gram-positive bacterial cell wall component that is spontaneously shed. The purpose of this study was to determine whether LTA could be quantified in biological samples and to evaluate potential relationships to markers of inflammation. Heparin-locked catheter aspirate was drawn from both the arterial and venous ports of each CVC prior to dialysis initiation. Venous blood from the dialysis circuit was collected 30 min after dialysis initiation. LTA was quantified in aspirate and plasma. Key markers of inflammation (interleukin-6, and hepcidin) and endothelial dysfunction (soluble vascular endothelial cadherin) were also determined in plasma samples. Catheter aspirate and systemic blood samples were obtained from 40 hemodialysis patients. The median (range) duration of catheter use was 130 (20–1635) days. Unexpectedly, median (range) plasma LTA concentrations (ng/mL) were significantly higher than catheter aspirate LTA concentrations [3.93 (0.25–15) vs. 2.38 (0.1–8.1), respectively, p = 0.01] in the majority (70%) of patients. Area under the receiver operator characteristic (ROC) curve showed good potential prognostic value of catheter aspirate LTA predicting systemic LTA concentrations with an area under the curve of 0.815 (95% CI, 0.68–0.95). A significant correlation was found between LTA and serum ferritin (r = 0.32, p = 0.04), however, there were no significant correlations between LTA and the other inflammation biomarkers assessed. LTA is quantifiable in aspirate and plasma of hemodialysis patients with CVCs and warrants further investigation to determine potential clinical application to intraluminal biofilm evaluation.

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Soluble vascular endothelial-cadherin and auto-antibodies to human vascular endothelial-cadherin in human diseases: Two new biomarkers of endothelial dysfunction

Cited by 23 publications

References 42 publications

Exposure to Zinc Oxide Nanoparticles Disrupts Endothelial Tight and Adherens Junctions and Induces Pulmonary Inflammatory Cell Infiltration

Exposure to Zinc Oxide Nanoparticles Disrupts Endothelial Tight and Adherens Junctions and Induces Pulmonary Inflammatory Cell Infiltration

Adenosine-to-Inosine Editing of Vasoactive MicroRNAs Alters Their Targetome and Function in Ischemia

Quantification of Lipoteichoic Acid in Hemodialysis Patients With Central Venous Catheters

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