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| Maresin 1 strengthen macrophages phagocytosis via miR-340 |
| XIE Haiqing, ZHANG Junli, XIE Xiang, JIN Shengwei. |
Department of Anesthesiology, the Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325027
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| Cite this article: |
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XIE Haiqing,ZHANG Junli,XIE Xiang, et al. Maresin 1 strengthen macrophages phagocytosis via miR-340[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2016, 46(5): 313-320,325.
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Abstract Objective: To investigate whether Maresin 1 (MaR1) could strengthen macrophage phagocytosis in sepsis model, and to explore the underlying mechanisms. Methods: Mouse peritoneal macrophages and bone marrow-derived macrophages (BMDMs) were assessed through detection of F4/80 expression by fluorescence microscopy and flow cytometry. MiR-340 expression was investigated under the treatment of MaR1 in CLP-induced and LPS-induced sepsis model in vivo and in vitro. MiR-340 expression in BMDMs transfected with miR-340 mimic or inhibitor was detected by quantificational real-time polymerase chain reaction (qRT-PCR). And then, the effect of miR-340 on phagocytosis of macrophage was investigated with fluorescence microscopy and flow cytometry. Finally, miR-340 serum concentration in sepsis patients and in healthy volunteers was measured. Results: Mouse peritoneal macropha-ges and BMDMs were consisted of approximately 90% as assessed by F4/80 expression. MiR-340 expression was up-regulated in LPS challenging and down-regulated with MaR1 administration in vivo and in vitro (P<0.05). MiR-340 expression was up-regulated in BMDMs transfected with miR-340 mimic, however dose not down-regulated in BMDMs transfected with miR-340 inhibitor. The phagocytosis of mouse peritoneal macrophages transfected with miR-340 mimic was suppressed by fluorescence microscopy (P<0.05); Similarly, the function of BMDMs transfected with miR-340 mimic was refrained by flow cytometry (P<0.05). MiR-340 serum concentration was elevated in sepsis patients (P<0.05). Conclusion: MaR1 can strengthen macrophage phagocytosis via miR-340 in sepsis.
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Received: 23 March 2016
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