Jianwei Sun1, Xijuan Wang1, Dandan Wang1, Ziyan Zhao1, Lei Zhang1, Jiajie Zhang2. 1. Neonatal Intensive Care Unit, Henan Provincial People's Hospital, Zhengzhou 450003, Henan, China. 2. Neonatal Intensive Care Unit, Henan Provincial People's Hospital, Zhengzhou 450003, Henan, China. Electronic address: zhangjj0060@126.com.
Abstract
BACKGROUND: The etiology of pneumonia is associated with gram-negative bacteria in malnourished children. To anatomize the molecular mechanisms, we focused on the modulatory function of circular RNA-Atp9b (circAtp9b) on inflammation in which microRNA-27a (miR-27a) might be implicated. METHODS: MRC-5 cells were stimulated by lipopolysaccharide (LPS) to exhibit inflammatory lesions assessed by viability and apoptosis as well as the cleavage of caspase-3, production of interleukin-6 and tumor necrosis factor alpha, and generation of reactive oxygen species (ROS). circAtp9b and miR-27a were quantified by qRT-PCR. circAtp9b- or miR-27a-silenced MRC-5 cells were established to study their roles in inflammation. Moreover, the change of NF-κB and JNK pathways was monitored. RESULTS: LPS was observed to induce adverse inflammatory injuries by repressing viability and fortified apoptosis with cleavage of caspase-3, production of cytokines, formation of ROS and abundance of circAtp9b. The results suggested circAtp9b silence prevented MRC-5 cells from LPS-elicited insults, which was accompanied by blockage of NF-κB and JNK. circAtp9b silence restored miR-27a which was repressed by LPS. miR-27a knockdown abrogated the protective capacities of circAtp9b silence with activation of NF-κB and JNK in response to LPS. CONCLUSION: LPS triggered adverse inflammation response by elevating the biogenesis of circAtp9b which caused a repressive role in miR-27a expression.
BACKGROUND: The etiology of pneumonia is associated with gram-negative bacteria in malnourished children. To anatomize the molecular mechanisms, we focused on the modulatory function of circular RNA-Atp9b (circAtp9b) on inflammation in which microRNA-27a (miR-27a) might be implicated. METHODS:MRC-5 cells were stimulated by lipopolysaccharide (LPS) to exhibit inflammatory lesions assessed by viability and apoptosis as well as the cleavage of caspase-3, production of interleukin-6 and tumor necrosis factor alpha, and generation of reactive oxygen species (ROS). circAtp9b and miR-27a were quantified by qRT-PCR. circAtp9b- or miR-27a-silenced MRC-5 cells were established to study their roles in inflammation. Moreover, the change of NF-κB and JNK pathways was monitored. RESULTS:LPS was observed to induce adverse inflammatory injuries by repressing viability and fortified apoptosis with cleavage of caspase-3, production of cytokines, formation of ROS and abundance of circAtp9b. The results suggested circAtp9b silence prevented MRC-5 cells from LPS-elicited insults, which was accompanied by blockage of NF-κB and JNK. circAtp9b silence restored miR-27a which was repressed by LPS. miR-27a knockdown abrogated the protective capacities of circAtp9b silence with activation of NF-κB and JNK in response to LPS. CONCLUSION:LPS triggered adverse inflammation response by elevating the biogenesis of circAtp9b which caused a repressive role in miR-27a expression.