Abstract
BackgroundGlobally, 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.ResultsLPS 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.ConclusionsOverexpression 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.
Highlights
Rhinitis is one of the most common chronic disorders
LPS induced cell injury and increased the expression of inflammatory cytokines in RPMI2650 cells Cell Counting Kit-8 (CCK-8) assay revealed that following treatment of RPMI2650 cells with LPS (5 μg/mL); the percentage of viable cells was significantly decreased (P < 0.05; Fig. 1a) compared to the control group
Flow cytometry revealed that the percentage of apoptotic cells was significantly increased (P < 0.001; Fig. 1b) following treatment of RPMI2650 cells with LPS (5 μg/mL) compared to the control group of cells
Summary
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. Rhinitis is one of the most common inflammatory disorders of the upper airways [1] This condition is triggered by exposure of the nasal mucosal cells to allergens. In addition to nasal obstruction, sense of itching and frequent sneezing, rhinitis is one of the important causes of disturbed sleep [1]. This condition is difficult to diagnose in young children [3]. Identification of the possible genetic and environmental mutagenicity factors, elucidation of the molecular pathways implicated in the pathogenesis of rhinitis, identification of novel drug targets, and improvement of current treatment strategies, remain the principal goal in rhinitis research [1,2,3]
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