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Modulation of epithelial tight junctions by TGF‐beta 3 in cultured oral epithelial cells
Author(s) -
Ye P
Publication year - 2012
Publication title -
australian dental journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.701
H-Index - 71
eISSN - 1834-7819
pISSN - 0045-0421
DOI - 10.1111/j.1834-7819.2011.01651.x
Subject(s) - tight junction , claudin , paracellular transport , barrier function , transforming growth factor , western blot , epithelium , microbiology and biotechnology , transforming growth factor beta , chemistry , cell junction , biology , permeability (electromagnetism) , gene , biochemistry , cell , genetics , membrane
Background: Previous studies have indicated that transforming growth factor beta 3 (TGF‐β3) was strongly expressed both in the gingival epithelium and the poorly structured pocket epithelium. Methods: A comprehensive analysis of the profile of tight junction proteins was carried out by quantitative real‐time RT‐PCR, Western blot and paracellular permeability assays. Results: Active TGF‐β3 protein added to monolayers of cultured oral epithelial cells initially reduced the permeability to dextran (10 kDa), followed by an increase in permeability. Three hours after the addition of TGF‐β3, expression of genes encoding tight junction components was selectively up‐ or down‐regulated. In addition, up‐ or down‐regulation of expression of several tight junction associated proteins was observed, although the protein changes did not parallel changes in gene expression. To confirm that TGF‐β3 plays a role in epithelial barrier function, a selective Src family kinase inhibitor saracatinib (AZD0530) was added to cells treated with active TGF‐β3. Tight junction proteins claudins‐2, ‐20 and ZO‐2 were significantly decreased, but claudin‐4 and ‐18 were significantly increased. Conclusions: These results suggest that TGF‐β3 is involved in the modulation of epithelial barrier function by regulating assembly of tight junctions.