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Departments of 1 Clinical Sciences and 2 Molecular Biomedical Sciences, North Carolina State University, Raleigh, North Carolina 27606
We have previously shown
that PGE2 and PGI2 induce recovery of
transepithelial resistance (TER) in ischemia-injured porcine ileal mucosa, associated with initial increases in Cl
secretion. We believe that the latter generates an osmotic gradient that stimulates resealing of tight junctions. Because of evidence implicating phosphatidylinositol 3-kinase (PI3K) in regulating tight
junction assembly, we postulated that this signaling pathway is
involved in PG-induced mucosal recovery. Porcine ileum was subjected to
45 min of ischemia, after which TER was monitored for a 180-min
recovery period. Endogenous PG production was inhibited with
indomethacin (5 µM). PGE2 (1 µM) and PGI2
(1 µM) stimulated recovery of TER, which was inhibited by serosal
application of the osmotic agent urea (300 mosmol/kgH2O).
The PI3K inhibitor wortmannin (10 nM) blocked recovery of TER in
response to PGs or mucosal urea. Immunofluorescence imaging of
recovering epithelium revealed that PGs restored occludin and zonula
occludens-1 distribution to interepithelial junctions, and this pattern
was disrupted by pretreatment with wortmannin. These experiments
suggest that PGs stimulate recovery of paracellular resistance via a
mechanism involving transepithelial osmotic gradients and
PI3K-dependent restoration of tight junction protein distribution.
phosphatidylinositol 3-kinase; tight junction; occludin; zonula occludens-1
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