Culture of murine brain microvascular endothelial cells that maintain expression and cytoskeletal association of tight junction-associated proteins

2003 ◽  
Author(s):  
li song ◽  
Joel Pachter
Keyword(s):  
Endothelial Cells ◽  
Tight Junction ◽  
Microvascular Endothelial Cells ◽  
Brain Microvascular Endothelial Cells ◽  
Associated Proteins ◽  
Murine Brain ◽  
Microvascular Endothelial

scholarly journals Caveolin-1 regulates expression of junction-associated proteins in brain microvascular endothelial cells

Blood ◽  
2006 ◽  
Vol 109 (4) ◽  
pp. 1515-1523 ◽  
Author(s):  
Li Song ◽  
Shujun Ge ◽  
Joel S. Pachter
Keyword(s):  
Endothelial Cells ◽  
Protein Expression ◽  
Adherens Junction ◽  
Microvascular Endothelial Cells ◽  
Brain Microvascular Endothelial Cells ◽  
Caveolin 1 ◽  
Synthetic Cell ◽  
Associated Proteins ◽  
Junctional Protein ◽  
Microvascular Endothelial

Abstract Recent evidence from this laboratory indicated that reduced expression of caveolin-1 accompanied the diminished expression of tight junction (TJ)–associated proteins occludin and zonula occludens-1 (ZO-1) following stimulation of brain microvascular endothelial cells (BMECs) with the chemokine CCL2 (formerly called MCP-1). Because attenuated caveolin-1 levels have also been correlated with heightened permeability of other endothelia, the objective of this study was to test the hypothesis that reduced caveolin-1 expression is causally linked to the action of CCL2 on BMEC junctional protein expression and barrier integrity. This was achieved using adenovirus to nondestructively deliver caveolin-1 siRNA (Ad-siCav-1) to BMEC monolayers, which model the blood-brain barrier (BBB). Treatment with siRNA reduced the caveolin-1 protein level as well as occludin and ZO-1. Additionally, occludin exhibited dissociation from the cytoskeletal framework. These changes were attended by comparable alterations in adherens junction (AJ)–associated proteins, VE-cadherin and β-catenin, increased BMEC paracellular permeability, and facilitated the ability of CCL2 to stimulate monocytic transendothelial migration. Furthermore, treating BMECs with cavtratin, a synthetic cell-permeable peptide encoding the caveolin-1 scaffolding domain, antagonized effects of both Ad-siCav-1 and CCL2. These results collectively highlight caveolin-1 loss as a critical step in CCL2-induced modulation of BMEC junctional protein expression and integrity, and possibly serve a crucial role in regulating inflammation at the BBB.

Adhesion molecules on murine brain microvascular endothelial cells: expression and regulation of ICAM-1 and Lgp 55

1992 ◽  
Vol 36 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Zsuzsanna Fabry ◽  
Mari M. Waldschmidt ◽  
Dana Hendrickson ◽  
Judy Keiner ◽  
Laurie Love-Homan ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecules ◽  
Microvascular Endothelial Cells ◽  
Brain Microvascular Endothelial Cells ◽  
Murine Brain ◽  
Microvascular Endothelial
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