Publication date: August 2018
Source:Biomedicine & Pharmacotherapy, Volume 104
Author(s): Jinjing Guo, Ying Cheng
ObjectiveThis study aimed to explore the potential roles and mechanism of miR-1247 in lipopolysaccharides (LPS)-induced acute pneumonia.Materials and methodsThe miR-1247 expression in acute stage patients with infantile pneumonia was detected. To establish the cell model of acute pneumonia, A549 cells were treated with 1 mg/mL lipopolysaccharides (LPS). The effects of miR-1247 dysregulation on the cell viability, apoptosis, inflammation and autophagy of LPS-induced A549 cells were investigated. Moreover, the functional targets of miR-1247 were identified and the regulatory relationships between miR-1247 and JNK or NF-κB pathways were explored.ResultsThe miR-1247 was lowly expressed in acute phage patients with infantile pneumonia. In addition, LPS treatment significantly inhibited A549cell viability, induced apoptosis, promoted the production of cytokines and decreased autophagy, thus causing A549 cell injury. Moreover, miR-1247 was decreased expression after LPS treatment, and overexpression of miR-1247 alleviated LPS-induced A549 cell injury. Furthermore, CC chemokine ligand (CCL) 16 was a functional target gene of miR-1247. Knockdown of CCL16 alleviated LPS-induced cell injury, and the combination of miR-1247 inhibition and CCL16 knockdown reversed the effects of CCL16 knockdown alone on LPS-induced A549 cell injury. Besides, inhibition of miR-1247 activated JNK and NF-κB pathways, while knockdown of CCL16 inhibited the activation of these pathways.ConclusionsOur data reveals that miR-1247 is lowly expressed in acute stage patients with infantile pneumonia. Overexpression of miR-1247 may alleviate LPS-induced A549 cell injury through targeting CCL16. JNK and NF-κB pathways may be key mechanisms to regulate the role of miR-1247 in LPS-induced lung injury.
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