Disease relevance of OCLN

• We examined whether hypoxia alone could produce changes in the permeability of brain capillary endothelial cells (EC) and whether a stimulation of hypoxic status alters the gene expression of occludin and glucose transporter 1 (GLUT1) [1].

High impact information on OCLN

• In vitro studies revealed that although PGE 2 induced Cl - secretion via at least 3 distinct secretory pathways, recovery of barrier function was initiated by Cl - secretion via ClC-2 Cl - channels co-expressed with occludin and localized to tight junctions within restituting epithelium [2].
• Reduced levels of the tight junction proteins claudin-1 and occludin accompanied the loss of barrier function [3].
• This dephosphorylation of occludin, occurring after activation of a serine/threonine kinase by TPA, suggested that protein kinase C was not acting directly on this tight junction target protein [4].
• As the phosphorylation state of occludin is thought to be important in both tight junction assembly and regulation, the effect of phorbol ester treatment on the phosphorylation of occludin was investigated [4].
• Surprisingly, activation of protein kinase C with 10(-7) M TPA resulted in a time-dependent decrease in threonine phosphorylation of occludin which correlated closely with the rapid decrease in transepithelial electrical resistance [4].

Biological context of OCLN

• Reverse transcription polymerase chain reaction (RT-PCR) was used to determine occludin and VEGF mRNA levels [5].

Anatomical context of OCLN

• Our data indicate that regulation of occludin expression may be a crucial determinant of the tight junction permeability properties of endothelial cells in different tissues [6].
• We also show that occludin expression is developmentally regulated, being low in rat brain endothelial cells at postnatal day 8 but clearly detectable at post-natal day 70 [6].
• Protein kinase C activation leads to dephosphorylation of occludin and tight junction permeability increase in LLC-PK1 epithelial cell sheets [4].
• In particular, localization of ZO-1 and ZO-2 expression moved from the cell membrane to the cytoplasm and nucleus whereas occludin expression remained at the cell membrane [7].

Associations of OCLN with chemical compounds

• Immunoblot analysis indicated that occludin levels in total cell lysates as well as cytosolic, membrane (Triton-X soluble) and cytoskeletal (Triton-X insoluble) fractions remained unchanged for at least 2 hours in cells treated with 10(-7) M TPA compared to their corresponding control cells [4].
• The mechanisms involve enhanced tyrosine phosphorylation and overexpression and possibly displacement or missorting of the junctional proteins occludin and E-cadherin [8].
• Furthermore, we found that interleukin-1 (IL-1)beta, glutamate, hydrogen peroxide (H2O2), and sodium nitroprusside (SNP) induced the expression of mRNA for occludin and GULT1 under normoxic condition [1].
• The expression level of occludin messenger RNA increased markedly immediately after the exposure to eicosapentaenoic acids or gamma linolenic acid [9].
• PAO-induced occludin proteolysis could be prevented by different MMP inhibitors [10].

Other interactions of OCLN

• These results indicate that the expression of occludin and GLUT1 mRNA is sensitive to exposure to hypoxia and that the changes of permeability in EC are associated with IL-1beta and NO [1].
• Immunofluorescence confocal microscopy revealed a broader staining of occludin and E-cadherin following IFNalpha treatment, with prominent staining at the basal cell pole in addition to localization at the junctional region [8].
• The tyrosine phosphatase inhibitor phenylarsine oxide (PAO) induced increased matrix metalloproteinase (MMP) activity, which was paralleled by severe disruption of cell-cell contacts and proteolysis of the tight junction protein occludin [10].
• Immunocytochemistry of PBCEC revealed a delocalisation of the cell border lining tight junction proteins ZO-1, occludin and claudin-5 when serum was added [11].
• In this study, the effects of shear stress on the expression of occludin and vascular endothelial growth factor (VEGF), two important regulators of endothelial permeability, were investigated [5].

Analytical, diagnostic and therapeutic context of OCLN

• In this study, we show, by immunocytochemistry, that occludin is present at high levels and is distributed continuously at cell-cell contacts in brain endothelial cells [6].
• The apparent differences in occludin expression levels were directly confirmed by immunoblotting [6].
• Immunofluorescence microscopy revealed a more rapid change in the membrane distribution of ZO-1 compared to occludin in the TPA-treated cells [4].
• Increased expression of occludin and E-cadherin was detected by Western blot analysis after IFNalpha treatment [8].
• The messenger RNA expression of occludin was quantitated by real-time quantitative reverse transcriptase-polymerase chain reaction [9].

References