Wang Kai, Zhang Nan
Department of Otolaryngology, Head and Neck Surgery, Southern University of Science and Technology Hospital, Shenzhen, China.
Department of Otolaryngology, Head and Neck Surgery, Shenzhen University General Hospital, Shenzhen, China.
Cell Biochem Biophys. 2025 Feb 14. doi: 10.1007/s12013-025-01689-3.
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.
探讨miR-634通过调控水通道蛋白5（AQP5）对脂多糖（LPS）诱导的人鼻上皮细胞（HNEpCs）炎症反应及凋亡的影响及潜在机制。采用qRT-PCR检测慢性鼻窦炎（CRS）患者组织及LPS诱导的HNEpCs中miR-634和AQP5的mRNA表达。采用蛋白质印迹法检测HNEpCs中AQP5的蛋白表达。通过流式细胞术评估细胞凋亡。采用CCK-8试剂盒检测细胞活力。结合生物信息学分析、双荧光素酶报告基因检测及蛋白质印迹法，预测并验证AQP5与miR-634之间的相互作用。结果表明，CRS组miR-634的mRNA表达显著上调，而AQP5下调。与对照组相比，CRS组AQP5的表达下调。体外实验表明，随着LPS浓度的增加，miR-634的表达逐渐增加，而AQP5逐渐降低。LPS诱导组细胞活力受到抑制，凋亡增加。此外，发现miR-634可抑制细胞活力并促进凋亡。qRT-PCR结果提示，miR-634上调LPS诱导的HNEpCs中炎症因子相关mRNA的表达。结合生物信息学分析和qRT-PCR，证实AQP5是miR-634的直接靶点。miR-634直接靶向AQP5调控CRS进展，包括抑制细胞活力、促进凋亡及加重炎症反应，这可能为其作为CRS治疗生物标志物的应用提供理论依据。
