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Related Experiment Videos

Kinin B1 receptor expression and function on human brain endothelial cells.

A Prat1, K Biernacki, S Pouly

  • 1Neuroimmunology Unit, Montreal Neurological Institute, McGill University, Quebec, Canada.

Journal of Neuropathology and Experimental Neurology
|November 18, 2000
PubMed
Summary

The kinin B1 receptor is inducible on human brain endothelial cells during inflammation. Signaling via this receptor increases blood-brain barrier permeability and alters chemokine production, impacting inflammatory responses.

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Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • The kinin B1 receptor is typically induced by inflammatory mediators.
  • Its presence and function on human brain endothelial cells (HBECs) are not well understood.

Purpose of the Study:

  • To investigate the expression of the kinin B1 receptor on HBECs.
  • To determine if kinin B1 receptor signaling affects HBEC permeability and chemokine production.

Main Methods:

  • Multiplex RT-PCR and Western blot were used to detect B1 receptor expression.
  • HBECs were stimulated with interferon-gamma and a selective B1 agonist (R-838).
  • Nitric oxide production, inositol triphosphate levels, and BSA permeability were measured.

Main Results:

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  • Interferon-gamma upregulated B1 receptor mRNA and protein on HBECs in a dose- and time-dependent manner.
  • B1 receptor activation increased nitric oxide and inositol triphosphate production.
  • B1 receptor activation significantly increased HBEC monolayer permeability and inhibited interleukin-8 release.

Conclusions:

  • Kinin B1 receptors can be upregulated on HBECs by inflammatory mediators.
  • Signaling through the B1 receptor influences blood-brain barrier permeability and chemokine production in vitro.