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P.O. Couraud

Researcher at French Institute of Health and Medical Research

Publications -  15
Citations -  2612

P.O. Couraud is an academic researcher from French Institute of Health and Medical Research. The author has contributed to research in topics: Blood–brain barrier & Signal transduction. The author has an hindex of 14, co-authored 15 publications receiving 2359 citations. Previous affiliations of P.O. Couraud include Paris Descartes University.

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Blood-brain barrier-specific properties of a human adult brain endothelial cell line

TL;DR: In this article, normal human brain endothelial cells were transduced by lentiviral vectors incorporating human telomerase or SV40 T antigen, and one was selected for expression of normal endothelial markers, including CD31, VE cadherin, and von Willebrand factor.
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BBB ON CHIP: microfluidic platform to mechanically and biochemically modulate blood-brain barrier function

TL;DR: The smallest model of the blood-brain barrier yet is presented, using a microfluidic chip, and the immortalized human brain endothelial cell line hCMEC/D3, which is very well suited to study barrier function and evaluate drug passage to finally gain more insight into the treatment of neurodegenerative diseases.
Journal Article

ICAM-1 Signaling Pathways Associated with Rho Activation in Microvascular Brain Endothelial Cells

TL;DR: The results suggest that through coupling to Rho activation and phosphorylation of cytoskeletal proteins and transcription factors, ICAM-1 cross-linking participates in the cell shape changes and gene regulation that may accompany lymphocyte migration through the blood-brain barrier.
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Expression of inflammatory genes induced by beta-amyloid peptides in human brain endothelial cells and in Alzheimer's brain is mediated by the JNK-AP1 signaling pathway.

TL;DR: Exposure of cultured human brain endothelial cells (HBEC) to Abeta elicited expression of inflammatory genes MCP-1, GRO, IL-1beta and IL-6 and suggested that JNK-AP1 signaling pathway is responsible for Abeta-induced neuroinflammation in HBEC and Alzheimer's brain and that this signaling pathway may serve as a therapeutic target for relieving AbETA-induced inflammation.
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Differences in amyloid-β clearance across mouse and human blood-brain barrier models: kinetic analysis and mechanistic modeling.

TL;DR: A modified form of the brain efflux index method was used and a mechanistic model was established, which could successfully predict cellular levels of (125)I-Aβ40 and the rate of each process, that describes Aβ clearance across BBB.