ArticleLaboratory investigation; a journal of technical methods and pathology2019
Multiplexed, high-throughput measurements of cell contraction and endothelial barrier function.
Article in Laboratory investigation; a journal of technical methods and pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Article
- Inferring cellular contractile forces and work using deep morphology traction microscopy.Biophysical journal · 2024Article
- A machine learning approach to predict cellular mechanical stresses in response to chemical perturbation.Biophysical journal · 2023Article
- Endothelial Poldip2 regulates sepsis-induced lung injury via Rho pathway activation.Cardiovascular research · 2022Article
- Article
- Paradigms of endothelial stiffening in cardiovascular disease and vascular aging.Frontiers in physiology · 2022Review
- Substrate stiffening promotes VEGF-A functions via the PI3K/Akt/mTOR pathway.Biochemical and biophysical research communications · 2022Article
- Apigenin and Ethaverine Hydrochloride Enhance Retinal Vascular Barrier In Vitro and In Vivo.Translational vision science & technology · 2020Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 4 countries.
Funding
Abstract
Vascular leakage, protein exudation, and edema formation are events commonly triggered by inflammation and facilitated by gaps that form between adjacent endothelial cells (ECs) of the vasculature. In such paracellular gap formation, the role of EC contraction is widely implicated, and even therapeutically targeted. However, related measurement approaches remain slow, tedious, and complex to perform. Here, we have developed a multiplexed, high-throughput screen to simultaneously quantify paracellular gaps, EC contractile forces, and to visualize F-actin stress fibers, and VE-cadherin. As proof-of-principle, we examined barrier-protective mechanisms of the Rho-associated kinase inhibitor, Y-27632, and the canonical agonist of the Tie2 receptor, Angiopoietin-1 (Angpt-1). Y-27632 reduced EC contraction and actin stress fiber formation, whereas Angpt-1 did not. Yet both agents reduced thrombin-, LPS-, and TNFα-induced paracellular gap formation. This unexpected result suggests that Angpt-1 can achieve barrier defense without reducing EC contraction, a mechanism that has not been previously described. This insight was enabled by the multiplex nature of the force-based platform. The high-throughput format we describe should accelerate both mechanistic studies and the screening of pharmacological modulators of endothelial barrier function.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.