MicroRNA-34a promotes iNOS secretion from pulmonary macrophages in septic suckling rats through activating STAT3 pathway.
Pediatric sepsis is frequently a fatal condition and a major cause of death globally. The mortality rate of sepsis remains high despite that the advanced therapeutic methods have been carried out. Our research aims to investigate the potentials of miR-34a in the treatment of pediatric sepsis. Results indicated that miR-34a was up-regulated in Lipopolysaccharide (LPS)-induced pulmonary macrophages and U937 cell lines. In addition, miR-34a silence reduced the production of iNOS through inactivating STAT3 pathway in U937 cell lines and cecal ligation and puncture (CLP)-induced lung tissues. Besides, high expression of iNOS and STAT3 in cells transfected with miR-34a mimic further validated it. Furthermore, in vivo experiment demonstrated that miR-34a silence protected CLP-induced suckling rats from lung injury. All in all, our study demonstrated that miR-34a promoted iNOS secretion from pulmonary macrophages in LPS-induced sepsis suckling rats through activating STAT3 pathway. These results provided a possibility to convert miR-34a into clinical application.
['Cheng|Dong-Liang|DL|', 'Fang|Hong-Xing|HX|', 'Liang|Yuan|Y|', 'Zhao|Yi|Y|', 'Shi|Chang-Song|CS|']
D000818:Animals D002432:Cecum D045744:Cell Line, Tumor D006801:Humans D008070:Lipopolysaccharides D008168:Lung D016676:Macrophages, Alveolar D035683:MicroRNAs D052247:Nitric Oxide Synthase Type II D051381:Rats D017207:Rats, Sprague-Dawley D050796:STAT3 Transcription Factor D018805:Sepsis D015398:Signal Transduction D020298:U937 Cells D015854:Up-Regulation
MicroRNA-34a iNOS Pulmonary macrophages STAT3 pathways Sepsis