Up‐regulation of the tight‐junction protein ZO‐1 by substance P and IGF‐1 in A431 cells

Abstract

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.

Strain-Dependent Augmentation of Tight-Junction Barrier Function in Human Primary Epidermal Keratinocytes by Lactobacillus and Bifidobacterium Lysates

“…Claudin 4 seals the paracellular space against the passage of ions and in doing so increases the TEER of monolayers (30,31). Increases in ZO-1 expression enhance the TEER of A431 cells (32), and the hormone GLP1 protects and also enhances TJ function in Caco-2 cells by increasing ZO-1 and occludin expression (33). The existence of TJs in skin has been discovered only relatively recently.…”

The K5 Capsule of Escherichia coli Strain Nissle 1917 Is Important in Stimulating Expression of Toll-Like Receptor 5, CD14, MyD88, and TRIF Together with the Induction of Interleukin-8 Expression via the Mitogen-Activated Protein Kinase Pathway in Epithelial Cells

“…The activation of the MAPK pathways by Nissle 1917 will contribute to its observed probiotic properties. It is known that Nissle 1917 inhibits gut leakage and promotes barrier function by enhancing tight junctions through increased ZO-1 expression (52) and that ZO-1 expression is ERK dependent (26). Likewise, among probiotic Lactobacillus species, MAPK-dependent signaling has been shown to be important in stimulating epithelial cell tight junctions and heat shock protein production (45,49).…”

Activation of transient receptor potential vanilloid subtype 1 increases expression and permeability of tight junction in normal and hyposecretory submandibular gland

“…1,2 Increased expression of ZO-1 is found to be associated with decreased paracellular permeability in the corneal and retinal pigment epithelium, 38,39 whereas the absence of ZO-1 results in a slight delay in the formation of TJ in MDCK cells and mouse mammary epithelial cells. 40 In MDCK I cells, the expression of Cldn-3 is not related with paracellular permeability, 41 whereas in gastric polarized epithelial cell line (MKN28), the knockdown expression of Cldn-3 induces a significant increase in paracellular permeability.…”