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Up‐regulation of the tight‐junction protein ZO‐1 by substance P and IGF‐1 in A431 cells
Author(s) -
Ko JiAe,
Murata Shizuka,
Nishida Teruo
Publication year - 2009
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1587
Subject(s) - mapk/erk pathway , tight junction , microbiology and biotechnology , kinase , a431 cells , barrier function , growth factor , epidermal growth factor , biology , phosphorylation , extracellular , chemistry , cell , receptor , cell cycle , biochemistry , oncogene
The formation of a barrier by tight junctions is important in epithelia of various tissues. Substance P (SP) and insulin‐like growth factor (IGF)–1 synergistically promote barrier function in the corneal epithelium. We have now examined the effects of SP and IGF‐1 on expression of the tight‐junction protein zonula occludens (ZO)–1 in A431 human epidermoid carcinoma cells. Reverse transcription–polymerase chain reaction (RT–PCR) and immunoblot analyses revealed that SP and IGF‐1 increased the amounts of ZO‐1 mRNA and protein in these cells in a concentration‐dependent manner, with neither SP nor IGF‐1 alone having such an effect. The SP‐ and IGF‐1–induced up‐regulation of ZO‐1 was accompanied by phosphorylation of extracellular signal–regulated kinase (ERK), and both of these effects were blocked by PD98059, an inhibitor of ERK activation. SP and IGF‐1 also increased the transepithelial electrical resistance (TER) (an indicator of barrier function) of an A431 cell monolayer in a manner sensitive to PD98059. Our results thus suggest that the synergistic induction of ZO‐1 expression by SP and IGF‐1 may promote barrier function in skin epithelial cells. Copyright © 2009 John Wiley & Sons, Ltd.