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Naji, M. |
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Motta, Antonella |
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Aletan, Dirar |
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Mohamed, Tarek |
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Ertürk, Emre |
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Taccardi, Nicola |
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Kononenko, Denys |
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Petrov, R. H. | Madrid |
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Alshaaer, Mazen | Brussels |
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Bih, L. |
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Casati, R. |
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Muller, Hermance |
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Kočí, Jan | Prague |
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Šuljagić, Marija |
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Kalteremidou, Kalliopi-Artemi | Brussels |
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Azam, Siraj |
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Ospanova, Alyiya |
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Blanpain, Bart |
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Ali, M. A. |
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Popa, V. |
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Rančić, M. |
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Ollier, Nadège |
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Azevedo, Nuno Monteiro |
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Landes, Michael |
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Rignanese, Gian-Marco |
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Wagner, Andreas
in Cooperation with on an Cooperation-Score of 37%
Topics
Publications (17/17 displayed)
- 2024Identification and Suppression of Point Defects in Bromide Perovskite Single Crystals Enabling Gamma-Ray Spectroscopycitations
- 2024Controlling Magneto‐Ionics by Defect Engineering Through Light Ion Implantationcitations
- 2024Controlling Magneto-Ionics by Defect Engineering Through Light Ion Implantationcitations
- 2024Positron annihilation analysis of nanopores and growth mechanism of oblique angle evaporated TiO2 and SiO2 thin films and multilayers
- 2023Ectodomain Shedding by ADAM17 Increases the Release of Soluble CD40 from Human Endothelial Cells under Pro-Inflammatory Conditions.citations
- 2022Ion Intercalation in Lanthanum Strontium Ferrite for Aqueous Electrochemical Energy Storage Devicescitations
- 2022Defect Nanostructure and its Impact on Magnetism of α-Cr2O3 thin filmscitations
- 2022Flexomagnetism and vertically graded Néel temperature of antiferromagnetic Cr2O3 thin films
- 2022Unravelling the Origin of Ultra‐Low Conductivity in SrTiO$_3$ Thin Films: Sr Vacancies and Ti on A‐Sites Cause Fermi Level Pinningcitations
- 2022Effect of Neutron Flux on an Irradiation-Induced Microstructure and Hardening of Reactor Pressure Vessel Steelscitations
- 2022Interface effect of Fe and Fe<sub>2</sub>O<sub>3</sub> on the distributions of ion induced defectscitations
- 2022Strongly enhanced growth of high-temperature superconducting films on an advanced metallic templatecitations
- 2021Mapping the structure of oxygen-doped wurtzite aluminum nitride coatings from ab initio random structure search and experimentscitations
- 2020Host-Guest Chemistry Meets Electrocatalysis:Cucurbit[6]uril on a Au Surface as a Hybrid System in CO 2 Reductioncitations
- 2020Host-Guest Chemistry Meets Electrocatalysis: Cucurbit[6]uril on a Au Surface as a Hybrid System in CO2 Reduction.
- 2018Voltage-controlled ON−OFF ferromagnetism at room temperature in a single metal oxide filmcitations
- 2018Voltage-controlled ON-OFF ferromagnetism at room temperature in a single metal oxide filmcitations
Places of action
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article
Ectodomain Shedding by ADAM17 Increases the Release of Soluble CD40 from Human Endothelial Cells under Pro-Inflammatory Conditions.
Abstract
<h4>Background</h4>Homozygosity for the C allele of the -1T>C single nucleotide polymorphism (SNP) of the <i>CD40</i> gene (rs1883832) is associated with susceptibility to coronary heart disease (CHD), enhanced CD40 expression, and shedding. The disintegrin metalloprotease ADAM17 can cleave various cell surface proteins. This study investigates an association between ADAM17-mediated CD40 shedding and inflammation in CC genotype human endothelial cells.<h4>Methods</h4>Human umbilical vein endothelial cells (HUVEC) carrying the CC genotype were stimulated with soluble CD40 ligand (sCD40L) or tumor necrosis factor-α (TNFα). Messenger RNA and protein expression were determined with standard methods. Levels of high sensitive c-reactive protein (hs-CRP), interleukin-6 (IL-6), and sCD40 in plasma samples from patients with CHD were assessed using ELISA.<h4>Results</h4>ADAM17 surface abundance was elevated following stimulation with CD40L and TNFα just as its regulator iRhom2. Inhibition of ADAM17 prevented TNFα-induced sCD40 and soluble vascular cell adhesion molecule-1 release into the conditioned medium and reinforced CD40 surface abundance. Secondary to inhibition of ADAM17, stimulation with CD40L or TNFα upregulated monocyte chemoattractant protein-1 mRNA and protein. Levels of sCD40 and the inflammatory biomarkers hs-CRP and IL-6 were positively correlated in the plasma of patients with CHD.<h4>Conclusions</h4>We provide a mechanism by which membrane-bound CD40 is shed from the endothelial cell surface by ADAM17, boosting sCD40 formation and limiting downstream CD40 signaling. Soluble CD40 may represent a robust biomarker for CHD, especially in conjunction with homozygosity for the C allele of the -1T>C SNP of the <i>CD40</i> gene.