miR-634 Mediated Aquaporin 5 Expression Regulates the Inflammatory Response and Apoptosis in Lipopolysaccharide-Induced Human Nasal Epithelial Cells.

Abstract

To investigate the effects and potential mechanism of miR-634 that regulates aquaporin 5 (AQP5) to regulate the inflammatory response and apoptosis in LPS-induced human nasal epithelial cells (HNEpCs). The mRNA expressions of miR-634 and AQP5 in the tissues of patients with chronic rhinosinusitis (CRS) and LPS-induced HNEpCs were detected by qRT-PCR. Western blotting was performed to detect the protein expression of AQP5 in HNEpCs. The apoptosis was assessed by flow cytometry. The cell viability was detected by CCK-8 kit. Combined with bioinformatics analysis, dual-luciferase reporter and western blotting, the interaction between AQP5 and miR-634 were predicted and verified. It proved that the mRNA expression of miR-634 in CRS group was significantly up-regulated, while AQP5 was down-regulated. And the expression of AQP5 in CRS group was down-regulated compared with control group. In vitro experiments indicated that the expression of miR-634 increased gradually, while AQP5 decreased gradually with the increase of LPS concentration. The cell viability was inhibited and apoptosis was promoted in LPS-induced group. In addition, it was found that miR-634 could inhibit cell viability and promote apoptosis. QRT-PCR results implied that miR-634 up-regulated the expression of inflammatory factor-related mRNA in LPS-induced HNEpCs. Combined with bioinformatics analysis and qRT-PCR, it was confirmed that AQP5 was the direct target of miR-634. MiR-634 directly targeted AQP5 to regulate CRS progression, including inhibiting cell viability, promoting apoptosis and aggravating inflammatory response, which may provide theoretical basis for its use as a biomarker for CRS treatment.