Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Regulation of Angiogenesis and Blood Supply

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...

T Cell Types and Functions

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Nectin receptors mediate mechanosensing to YAP via AKT.

Communications biology·2026

Same author

CoCB cell signalling 2024.

Current opinion in cell biology·2026

Same author

A rapid method of evaluating cytotoxic drug efficacy using sub-cellular fluctuation imaging.

Scientific reports·2025

Same author

Phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) inhibitors reduce vascular inflammation in vitro and in vivo.

British journal of pharmacology·2025

Same author

Sos1 ablation alters focal adhesion dynamics and increases Mmp2/9-dependent gelatinase activity in primary mouse embryonic fibroblasts.

Cell communication and signaling : CCS·2025

Same author

Pharmacological inhibition of ezrin reduces proliferative and invasive phenotype in acute lymphoblastic leukemia cells.

European journal of pharmacology·2024

Search research articles

Related Experiment Video

Updated: Jun 15, 2026

On-Chip Endothelial Inflammatory Phenotyping

On-Chip Endothelial Inflammatory Phenotyping

Published on: July 21, 2012

CD73 represses pro-inflammatory responses in human endothelial cells.

Jana Kg Grünewald¹, Anne J Ridley

¹King's College London, Randall Division of Cell and Molecular Biophysics, New Hunt's House, Guy's Campus, London SE1 1UL, UK. anne.ridley@kcl.ac.uk.

Journal of Inflammation (London, England)

|February 26, 2010

Summary

CD73 depletion in human endothelial cells significantly reduces adenosine production and promotes pro-inflammatory responses, including increased leukocyte adhesion and altered cell morphology. These findings reveal CD73

More Related Videos

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response

Published on: September 15, 2017

Related Experiment Videos

Last Updated: Jun 15, 2026

On-Chip Endothelial Inflammatory Phenotyping

On-Chip Endothelial Inflammatory Phenotyping

Published on: July 21, 2012

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response

Published on: September 15, 2017

Area of Science:

Endothelial cell biology
Immunology
Biochemistry

Background:

CD73 is an enzyme producing extracellular adenosine, influencing cellular responses via purinergic receptors.
Previous studies suggested CD73 regulates pro-inflammatory molecules in mouse endothelium.
The precise role of CD73 in human endothelial cells remained to be elucidated.

Purpose of the Study:

To investigate the function of CD73 in human endothelial cells.
To determine the impact of CD73 depletion on endothelial cell responses.

Main Methods:

Utilized RNA interference (RNAi) to deplete CD73 levels in human umbilical cord endothelial cells (HUVECs).

Main Results:

CD73 depletion markedly reduced extracellular adenosine production, confirming CD73 as the primary source.
Depletion of CD73 mimicked pro-inflammatory cytokine TNF-alpha effects, increasing leukocyte adhesion molecules (ICAM-1, VCAM-1, E-selectin) and NF-kB translocation.
CD73-depleted cells exhibited morphological changes, including elongation, increased stress fibers, and enhanced endothelial permeability, similar to TNF-alpha treated cells.

Conclusions:

CD73 plays a crucial role in suppressing pro-inflammatory responses in human endothelial cells.
The findings highlight CD73 as a potential therapeutic target for inflammatory conditions affecting the endothelium.