Abstract
Epithelial barrier integrity is critical to maintain the homeostasis in the body. The regulatory mechanism of the epithelial barrier function has not been fully understood. This study aims to elucidate the role of the TWIK-related potassium channel-1 (Trek1) in the regulation of the epithelial barrier function of the nasal mucosa. In this study, the levels of Trek1 were assessed by real time RT-PCR and Western blotting. The epithelial barrier function of the rat nasal epithelia was evaluated by the Ussing chamber system. The results showed that Trek1 was detected in the human and rat nasal epithelia, which were significantly lower in patients and rats with allergic rhinitis than that in healthy controls. Exposure to the signature T helper 2 cytokine, interleukin (IL)-4, markedly suppressed the expression of Trek1 in the nasal mucosa via up regulating the expression of the histone deacetylase (HDAC)1. The IL-4-induced rat nasal epithelial barrier dysfunction could be blocked by HDAC1 inhibitor (Trichostatin A), or sodium butyrate, or administration of Clostridium Butyricum. We conclude that Trek1 is critical to maintain the nasal epithelial barrier function.Electronic supplementary materialThe online version of this article (doi:10.1038/srep09191) contains supplementary material, which is available to authorized users.
Highlights
Epithelial barrier integrity is critical to maintain the homeostasis in the body
The results showed that Trek[1] was detected in the normal nasal epithelia, which was much less in the specimens from allergic rhinitis (AR) patients (Fig. 1)
The results indicate that the expression of Trek[1] is suppressed in the nasal mucosa with allergic disorders, which is in parallel to the nasal epithelial barrier dysfunction
Summary
Epithelial barrier integrity is critical to maintain the homeostasis in the body. The regulatory mechanism of the epithelial barrier function has not been fully understood. This study aims to elucidate the role of the TWIK-related potassium channel-1 (Trek1) in the regulation of the epithelial barrier function of the nasal mucosa. In the former case, the paracellular space may be enlarged by losing tight junction associated proteins[2,7], or increasing in the expression of some tight junction associating proteins, such as claudin 28 In the latter case, the endocytic molecules are not properly decomposed in the epithelial cells, such as deficiency of ubiquitin A209, resulting in the macromolecular proteins or peptides with functional antigenicity to be transported across the epithelial barrier to reach the subepithelial region. Earlier studies of the expression and function of TREK 1 are more concentrated in neural systems[14,15], recent studies showed that TREK 1 expression in endothelial cells mediated vasodilation and local regulation[16]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
