Abstract：Objective To explore the effects of miR-221 on the inflammatory factor secretion from macrophages after Mycobacterium tuberculosis infection. Methods The expression of miR-221 in macrophages after Mycobacterium tuberculosis infection was detected by real-time quantitative PCR (qRT-PCR). Macrophages were transiently transfected with miR-221 mimic or miR-221 inhibitor. The expression of macrophage inflammatory factor and secretion of NO were detected by enzyme-linked immunosorbent assay (ELISA) and Griess method, respectively. The relationship of miR-221 and Rho-associated, coiled-coil containing protein kinase 1 (ROCK1) was analyzed by dual-luciferase reporter gene assay, qRT-PCR and Western blot. Results Down-regulated miR-221 was observed in macrophages infected with Mycobacterium tuberculosis. The expression of miR-221 in macrophages was up-regulated by miR-221 mimics, but down-regulated by miR-221 inhibitors. The secretions of TNF-α, IL-1β, IL-6 and NO were significantly accelerated in macrophages infected with Mycobacterium tuberculosis, and increased in miR-221 up-regulated macrophages, but suppressed in miR-221 down-regulated macrophages. miR-221 directly binds to the 3′UTR of ROCK1, and negatively regulated its expression. Conclusion miR-221 can regulate the ROCK1 expression and inhibit the secration of inflammatory factors expression in macrophages after Mycobacterium tuberculosis infection.
何宝明 柏莹 李艳琴. miR-221对结核分枝杆菌感染巨噬细胞后炎性因子表达的影响[J]. 中国医药导报, 2018, 15(24): 14-17,29.
HE Baoming BAI Ying LI Yanqin. Effects of miR-221 on the inflammatory factor secretion from macrophages after Mycobacterium tuberculosis infection. 中国医药导报, 2018, 15(24): 14-17,29.
[1] Mjid M，Cherif J，Ben Salah N，et al. Epidemiology of tuberculosis [J]. Rev Pneumol Clin，2015，71（2/3）：67-72.
[2] Liu HY. Down-regulation of miR-144 after Mycobacterium tuberculosis infection promotes inflammatory factor secretion from macrophages through the Tpl2/ERK pathway [J]. Cell Mol Biol（Noisy-le-grand），2016，62（2）：87-93.
[3] 程涛，伍伟玲，黄河.肺结核患者Th1/Th2/Treg/Th17免疫应答的临床研究[J].中国医药导报，2017，14（26）：109-112.
[4] Marques-Rocha JL，Samblas M，Milagro FI，et al. Noncoding RNAs，cytokines，and inflammation-related diseases [J]. FASEB J，2015，29（9）：3595-3611.
[5] Chen CF，Huang J，Li H，et al. MicroRNA-221 regulates endothelial nitric oxide production and inflammatory response by targeting adiponectin receptor 1 [J]. Gene，2015， 565（2）：246-251.
[6] Ni B，Rajaram MV，Lafuse WP，et al. Mycobacterium tuberculosis decreases human macrophage IFN-gamma responsiveness through miR-132 and miR-26a [J]. J Immunol，2014，193（9）：4537-4547.
[7] Barry SE，Chan B，Ellis M，et al. Identification of miR-93 as a suitable miR for normalizing miRNA in plasma of tuberculosis patients [J]. J Cell Mol Med，2015，19（7）：1606-1613.
[8] Lundqvist-Gustafsson H，Norrman S，Nilsson J，et al. Involvement of p38-mitogen-activated protein kinase in Staphylococcus aureus-induced neutrophil apoptosis [J]. J Leukoc Biol，2001，70（4）：642-648.
[9] Schlesinger LS. Macrophage phagocytosis of virulent but not attenuated strains of Mycobacterium tuberculosis is mediated by mannose receptors in addition to complement receptors [J]. J Immunol，1993，150（7）：2920-2930.
[10] Torres-Juarez F，Cardenas-Vargas A，Montoya-Rosales A，et al. LL-37 immunomodulatory activity during Mycobacterium tuberculosis infection in macrophages [J]. Infect Immun，2015，83（12）：4495-4503.
[11] Huang S，Robinson JB，Deguzman A，et al. Blockade of nuclear factor-kappaB signaling inhibits angiogenesis and tumorigenicity of human ovarian cancer cells by suppressing expression of vascular endothelial growth factor and interleukin 8 [J]. Cancer Res，2000，60（19）：5334-5339.
[12] Xu Z，Zhou A，Ni J，et al. Differential expression of miRNAs and their relation to active tuberculosis [J]. Tuberculosis，2015，95（4）：395-403.
[13] Kleinsteuber K，Heesch K，Schattling S，et al. Decreased expression of miR-21，miR-26a，miR-29a，and miR-142-3p in CD4（+）T cells and peripheral blood from tuberculosis patients [J]. PLoS one，2013，8（4）：e61609.
[14] Li M，Wang J，Fang Y，et al. microRNA-146a promotes mycobacterial survival in macrophages through suppressing nitric oxide production [J]. Sci Rep，2016，6：24555.
[15] Forgione N，Fehlings MG. Rho-ROCK inhibition in the treatment of spinal cord injury [J]. World Neurosurg，2014， 82（3/4）：e535-e539.
[16] Zhao S，Zhang Y，Chen Q，et al. A modified "double-hit" induced acute lung injury model in rats and protective effects of tetramethylpyrazine on the injury via Rho/ROCK pathway [J]. Int J Clin Exp Pathol，2015，8（5）：4581-4587.
[17] He K，Yan L，Pan CS，et al. ROCK-dependent ATP5D modulation contributes to the protection of notoginsenoside NR1 against ischemia-reperfusion-induced myocardial injury [J]. Am J Physiol Heart Circ Physiol，2014， 307（12）：H1764-H1776.
[18] Arevalos CA，Walborn AT，Rupert AA，et al. Regulation of valve endothelial cell vasculogenic network architectures with ROCK and Rac inhibitors [J]. Microvasc Res，2015，98：108-118.
[19] Liu D，Xiong R，Chen X，et al. The glucocorticoid dexamethasone inhibits U937 cell adhesion and neutrophil release via RhoA/ROCK1-dependent and independent pathways [J]. Cell Physiol Biochem，2014，33（6）：1654-1662.
[20] Moon HG，Cao Y，Yang J，et al. Lung epithelial cell-derived extracellular vesicles activate macrophage-mediated inflammatory responses via ROCK1 pathway [J]. Cell Death Dis，2015，6：e2016.
2018, Vol. 15 
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