We also demonstrate that NS1 from DENV1, DENV2, DENV3, and DENV4 triggers endothelial barrier dysfunction, causing increased permeability
of human endothelial cell monolayers in vitro.
The researchers used the power of gene sequencing and clever computational methods to uncover the «source code»
for human endothelial cells and learn how that code is disturbed in human disease.
Professor Takao Hamakubo's group at the Department of Quantitative Biology and Medicine, Research Center for Advanced Science and Technology (RCAST), have shown that PTX3 forms strong bonds with histones and partially unfolds, leading to a disordered coaggregation of histone and PTX3 and
protecting human endothelial cells from damage.
Says Deosarkar, «In this study, we have developed a first realistic pediatric BBB model (B3C) using RBECs from rat pups and
human endothelial cells which could serve as an in vitro model system for studying BBB function in pediatric neurological diseases as well as for testing novel therapies for these diseases.»
By culturing RBECs and
human endothelial cells under flow conditions, the researchers found that cell - cell junctions they formed accurately mimicked endothelial barrier formation in the brain.
Researchers from KTH Royal Institute of Technology, Karolinska Institutet and University Medical Centre Hamburg - Eppendorf, in collaboration with the Human Protein Atlas Project, worked with a systems - based approach to identify a large panel of genes predominantly expressed
in human endothelial cells.
The protein, they found, preferentially binds to
human endothelial cells, allowing the retrovirus, which would not normally infect human cells, to enter them.
Now bioengineering researchers at Temple University in Philadelphia have come up with an experimental workaround — a synthetic pediatric blood - brain barrier on a small chip — and have tested it successfully using rat brain endothelial cells (RBECs) from rat pups and
human endothelial cells.
To understand this phenomenon better, the regenerative properties of
human endothelial cells have been studied extensively [1,4 - 6].
Magnesium deficiency was shown to speed up the death of
human endothelial cells and fibroblasts, leading to accelerated aging and age - related diseases.