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endothelial cells

HDAC11 Promotes Both NLRP3/Caspase-1/GSDMD and Caspase-3/GSDME Pathways Causing Pyroptosis via ERG in Vascular Endothelial Cells

[Cell Death Discovery] Researchers investigated the role of histone deacetylase 11 (HDAC11) in vascular endothelial cell pyroptosis and its molecular mechanism.

Role of Swiprosin-1/EFHD2 as a Biomarker in the Development of Chronic Diseases

[Life Sciences] The aim of this review is to summarize and provide an overview of the role of swiprosin-1 in pathophysiological conditions of cancers, cardiovascular diseases, diabetic nephropathy, neuropsychiatric diseases, and in the process of inflammation, immune response, and inflammatory diseases.

Structural Basis for HCMV Pentamer Receptor Recognition and Antibody Neutralization

[Science Advances] Investigators determined the structures of Pentamer bound to neuropilin 2 and a set of potent neutralizing antibodies against human cytomegalovirus (HCV).

Intercellular Transfer of miR-200c-3p Impairs the Angiogenic Capacity of Cardiac Endothelial Cells

[Molecular Therapy] Researchers reported that cardiac stress-induced differential microRNA content, with miR-200c-3p being one of the most enriched, in cardiomyocyte-derived extracellular vesicles mediates functional crosstalk with endothelial cells.

Elucidating Mechanisms of Genetic Cross-Disease Associations at the PROCR Vascular Disease Locus

[Nature Communications] Using genetic analysis, human recall-by-genotype and in vitro experimentation, researchers demonstrated that PROCR-219Gly increased plasma levels of (activated) protein C through endothelial protein C receptor ectodomain shedding in endothelial cells, attenuating leukocyte–endothelial cell adhesion and vascular inflammation.

The Suppressive Effects of Mer Inhibition on Inflammatory Responses in the Pathogenesis of LPS-Induced ALI/ARDS

[Science Signaling] In human pulmonary aortic endothelial cells,lipopolysaccharide (LPS) induced decreased in the amounts of endothelial nitric oxide synthase, thrombomodulin, and vascular endothelial–cadherin, which was blocked by treatment with UNC2250.

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