MicroRNA-34a promotes iNOS secretion from pulmonary macrophages in septic suckling rats through activating STAT3 pathway - 11/07/18
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Graphical abstract |
Highlights |
• | Elevated level of miR-34a was observed in LPS-induced sepsis rats and U937. |
• | miR-34a was positively related to iNOS production in LPS-induced macrophages. |
• | miR-34a induced iNOS+ productions through STAT3 nucleus translocation. |
• | miR-34a silence protects CLP-induced sepsis rats from pulmonary injury. |
Abstract |
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.
Le texte complet de cet article est disponible en PDF.Abbreviations : LPS, miRNAs, CLP, iNOS, JAK/STAT3, p-STAT3
Keywords : MicroRNA-34a, iNOS, Pulmonary macrophages, Sepsis, STAT3 pathways
Plan
Vol 105
P. 1276-1282 - septembre 2018 Retour au numéro
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