Central Research Laboratory, Institute of Medical Science, The Second Hospital of Shandong University, Shandong University, Jinan, Shandong Province, China.
Key Laboratory of Marine Drugs, Chinese Ministry of Education, School of Medicine and Pharmacy, Ocean University of China, Qingdao, 266003, China.
Inflammation. 2019 Aug;42(4):1389-1400. doi: 10.1007/s10753-019-01000-6.
Chronic nasal sinusitis with nasal polyps (CRSwNP) is a reversible nasal mucosal remodeling disease caused by persistent inflammation and structural changes in chronic nasal mucosa. Although there have been many studies on the inflammation of the nasal mucosa epithelium, the mechanism remains unclear. Our study found that H3K4me3 histone demethylase KDM2B (also known as JHDM1B) and transcriptional regulator Brg1 (also called SNF2-β or Smarca4) were significantly decreased in nasal mucosa of CRSwNP patients, and they were positively correlated. Brg1 and KDM2B co-localize in the epithelial cells of nasal mucosa. We used poly(I:C)-treated nasal mucosal epithelial cells (HNECs) to find that the expression of KDM2B and Brg1 was also decreased, and the main expression position transferred from the nucleus to the nuclear membrane. We used small interfering RNA to knock down the expression of KDM2B and Brg1 in nasal epithelial cells. It was interesting to find that the decreased expression of KDM2B and Brg1 produced similar effects to that of poly(I:C)-treated cells, which could promote inflammatory response of nasal mucosal epithelial cells. And Brg1 appears to play a role in KDM2B regulating gene promoters of IL-6 and TNF-α inflammatory. This study shows that KDM2B and Brg1 may have an inhibitory effect on the development of CRSwNP nasal mucosal epithelial inflammation. This study will provide a new perspective for gene targeting therapy of CRSwNPs.
慢性鼻-鼻窦炎伴鼻息肉(CRSwNP)是一种由慢性鼻黏膜持续性炎症和结构改变引起的可逆转的鼻黏膜重塑性疾病。尽管已经有许多关于鼻黏膜上皮炎症的研究,但机制仍不清楚。我们的研究发现,CRSwNP 患者鼻黏膜中的 H3K4me3 组蛋白去甲基化酶 KDM2B(也称为 JHDM1B)和转录调节因子 Brg1(也称为 SNF2-β 或 Smarca4)显著减少,且呈正相关。Brg1 和 KDM2B 在鼻黏膜上皮细胞中共定位。我们使用多聚(I:C)处理鼻黏膜上皮细胞(HNECs)发现,KDM2B 和 Brg1 的表达也降低了,其主要表达位置从细胞核转移到核膜。我们使用小干扰 RNA 敲低鼻上皮细胞中的 KDM2B 和 Brg1 的表达。有趣的是,发现 KDM2B 和 Brg1 的表达降低产生了类似于多聚(I:C)处理细胞的效果,可促进鼻黏膜上皮细胞的炎症反应。而 Brg1 似乎在 KDM2B 调节 IL-6 和 TNF-α 炎症相关基因启动子方面发挥作用。本研究表明,KDM2B 和 Brg1 可能对 CRSwNP 鼻黏膜上皮炎症的发展具有抑制作用。本研究将为 CRSwNPs 的基因靶向治疗提供新视角。