Trek1 contributes to maintaining nasal epithelial barrier integrity

• DOI: 10.1038/srep09191
• Publication Date: 2015-03-17T10:15:56Z
• Authors: Jing Jiang; Jiang-Qi Liu; Jing Li; Meng Li; Hong-Bin Chen; Hao Yan; Li-Hua Mo; Shu-Qi Qiu; Zhi-Gang Liu; Ping-Chang Yang
• Keywords: 0301 basic medicine; 0303 health sciences; Gene Expression; Histone Deacetylase 1; Immunohistochemistry; Rhinitis, Allergic; Article; Rats; 3. Good health; Histone Deacetylase Inhibitors; Disease Models, Animal; Nasal Mucosa; 03 medical and health sciences; Potassium Channels, Tandem Pore Domain; Th2 Cells; Case-Control Studies; Animals; Cytokines; Humans; Female; History, Ancient

AbstractEpithelial 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.