Teng Yaoshu, Zhang Ruxin, Liu Chunhui, Zhou Lingling, Wang Hong, Zhuang Wenjie, Huang Yu, Hong Zhicong
Department of Otolaryngology, Huadong Hospital, Fudan University, Shanghai 200040, China.
Department of Otolaryngology, Huadong Hospital, Fudan University, Shanghai 200040, China.
Biochem Biophys Res Commun. 2015 Jan 30;457(1):58-64. doi: 10.1016/j.bbrc.2014.12.058. Epub 2014 Dec 18.
Allergic rhinitis (AR) is a common chronic inflammatory condition of the nasal mucosal tissue. The interleukin-13 (IL-13) signaling pathway is of great importance in the pathogenesis of AR. However, how the signaling molecules in this pathway are regulated, particularly through microRNAs (miRNAs), remains unclear. In the present study, we investigated the regulatory role and mechanism of miRNA-143 (miR-143) in IL-13-induced inflammatory cytokine and mucus production in nasal epithelial cells (NECs) from AR patients. Our results showed that forced expression of miR-143 significantly decreased the mRNA and protein expression levels of granulocyte-macrophage colony-stimulating factor (GM-CSF), eotaxin and mucin 5AC (MUC5AC) in IL-13-stimulated NECs. Moreover, we confirmed that miR-143 directly targeted and significantly suppressed IL-13 receptor α1 chain (IL13Rα1) gene expression. This study thus suggests that miR-143 regulation of IL-13-induced inflammatory cytokine and mucus production in NECs from AR patients probably partly depends on inhibition of IL13Rα1. Therefore, the IL13Rα1 signaling pathway may be a potential target for the prevention and treatment of AR by miR-143.
变应性鼻炎（AR）是鼻黏膜组织常见的慢性炎症性疾病。白细胞介素13（IL-13）信号通路在AR发病机制中至关重要。然而，该通路中的信号分子如何受到调控，尤其是通过微小RNA（miRNA）进行调控，仍不清楚。在本研究中，我们调查了miRNA-143（miR-143）对AR患者鼻上皮细胞（NECs）中IL-13诱导的炎性细胞因子及黏液产生的调控作用和机制。我们的结果表明，在IL-13刺激的NECs中，miR-143的强制表达显著降低了粒细胞-巨噬细胞集落刺激因子（GM-CSF）、嗜酸性粒细胞趋化因子和黏蛋白5AC（MUC5AC）的mRNA及蛋白表达水平。此外，我们证实miR-143直接靶向并显著抑制IL-13受体α1链（IL13Rα1）基因的表达。因此，本研究提示，miR-143对AR患者NECs中IL-13诱导的炎性细胞因子及黏液产生的调控可能部分依赖于对IL13Rα1的抑制作用。所以，IL13Rα1信号通路可能是miR-143预防和治疗AR的潜在靶点。
