Huang Nan, Li Wenjing, Wang Xiaolong, Qi Shanshan
Department of Allergy, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Department of Allergy, Wuhan No.1 Hospital, No. 215, Zhongshan Avenue, Wuhan, 430022, China.
BMC Cell Biol. 2018 Feb 13;19(1):1. doi: 10.1186/s12860-018-0152-5.
Globally, rhinitis is one of the most common chronic disorders. Despite availability of drugs to manage the symptomatology of rhinitis, researchers still focus on identification of novel molecular targets for better management. MicroRNAs are implicated in many biological and pathological processes. However, the role of miR-17-5p in rhinitis remains unexplored. This study aimed to explore the role of miR-17-5p in lipopolysaccharide (LPS)-induced injury of nasal epithelial RPMI2650 cells and to elucidate the possible underlying molecular mechanism.
LPS damaged RPMI2650 cells by inhibiting cell proliferation, promoting apoptosis, and stimulating the release of inflammatory cytokines. miR-17-5p expression was significantly increased in RPMI2650 cells following treatment with LPS. Furthermore, it was found that overexpression of miR-17-5p led to aggravation of LPS-induced injury. miR-17-5p negatively regulated expression of Smad7; overexpression of Smad7 protected the RPMI2650 cells by inactivating NF-κB and Wnt/β catenin pathways and vice versa.
Overexpression of miR-17-5p aggravated LPS-induced damage of RPMI2650 cells. Expression of Smad7 was negatively regulated by miR-17-5p; Smad7 expression inactivated NF-κB and Wnt/β catenin pathways.
在全球范围内，鼻炎是最常见的慢性疾病之一。尽管有药物可用于控制鼻炎的症状，但研究人员仍专注于寻找新的分子靶点以实现更好的治疗。微小RNA参与许多生物学和病理过程。然而，miR-17-5p在鼻炎中的作用仍未得到探索。本研究旨在探讨miR-17-5p在脂多糖（LPS）诱导的鼻上皮RPMI2650细胞损伤中的作用，并阐明可能的潜在分子机制。
LPS通过抑制细胞增殖、促进细胞凋亡和刺激炎性细胞因子的释放来损伤RPMI2650细胞。用LPS处理后，RPMI2650细胞中miR-17-5p的表达显著增加。此外，发现miR-17-5p的过表达导致LPS诱导的损伤加重。miR-17-5p负向调节Smad7的表达；Smad7的过表达通过使NF-κB和Wnt/β连环蛋白通路失活来保护RPMI2650细胞，反之亦然。
miR-17-5p的过表达加重了LPS诱导的RPMI2650细胞损伤。miR-17-5p负向调节Smad7的表达；Smad7的表达使NF-κB和Wnt/β连环蛋白通路失活。
