BACKGROUND: Vascular permeability is controlled by endothelial cell-to-cell junctions. @entity3545 , the major component of adherence junctions (AJ) in the endothelium, is the target of the permeability-increasing agent @entity5 @entity39 factor-a ( @entity310 ). We investigated whether @entity310 regulates the synthesis of @entity3545 on the transcriptional level. MATERIALS AND METHODS: @entity1 endothelial cells, isolated from aorta (aEC) and umbilical cord (HUVEC), were exposed to @entity310 (200 U/ml) for 6 h or 12 h, with and without subsequent incubation with @entity310 for 24 h. @entity3545 mRNA was evaluated by semi-quantitative RT-PCR. The @entity3545 protein expression was analyzed by flow cytometry (FACS). RESULTS: The @entity3545 amplification curve of @entity310 treated cells was shifted to the right compared to controls, indicating a lower mRNA amount. The number of cycles at which half-maximal amplification (N50) was achieved, was lower for control aEC (30.7) than for @entity310 treated aEC (33.0). The N50 of HUVEC treated with @entity310 for 12 h and 12 h + 24 h medium (N50 = 32.1), was higher compared to controls (N50 = 29.7) and cells treated with @entity310 for 6 h (N50 = 30.8). As determined by FACS analysis, incubation with @entity310 caused a small decrease of @entity3545 protein expression from 7.44 to 6.05 mean channel intensity. CONCLUSION: Our results indicate that @entity310 affects @entity3545 gene expression on the transcriptional level, inducing a downregulation of the @entity3545 expression.

The @entity5 @entity39 factor-alpha induced vascular permeability is associated with a reduction of XXXX expression.

@entity1 :: ('9606', 'Species') :: ['Human'] @entity39 :: ('MESH:D009336', 'Disease') :: ['necrosis'] @entity5 :: ('MESH:D009369', 'Disease') :: ['tumour'] @entity310 :: ('7124', 'Gene') :: ['TNF-alpha'] @entity3545 :: ('1003', 'Gene') :: ['VE-cadherin', 'Vascular endothelial (VE)-cadherin', 'VE-Cadherin']
@entity3545 :: (1003,Gene) :: ['VE-cadherin']
