MicroRNA-155 Participates in Smoke-Inhalation-Induced Acute Lung Injury through Inhibition of SOCS-1
MicroRNA-155 Participates in Smoke-Inhalation-Induced Acute Lung Injury through Inhibition of SOCS-1
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MicroRNA-155 通过抑制 SOCS-1 参与烟雾吸入诱发的急性肺损伤
DOI：
10.3390/molecules25051022
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发表时间：
2020-02
期刊：
影响因子：
4.6
通讯作者：
Zhao Hang
中科院分区：
文献类型：
--
作者：
Zhang Yue;Xie Yifang;Zhang Leifang;Zhao Hang
烟雾吸入引起急性肺损伤是一种严重的临床疾病，死亡率高。越来越多的证据表明，microRNA-155 （miR-155）和细胞因子信号传导抑制因子1 （SOCS-1）作为炎症反应的介质，参与了ALI的发病过程。在本文中，我们探讨了miR-155在烟雾吸入诱导ALI中的促炎机制。我们的数据显示，烟雾吸入诱导miR-155表达，miR-155敲除（KO）显著改善烟雾吸入诱导的小鼠肺损伤。吸入烟雾后，miR-155（-/-）小鼠的中性粒细胞浸润和髓过氧化物酶（MPO）、巨噬细胞炎症蛋白2 （MIP-2）和角化细胞趋化剂（KC）的表达也降低。Real-time RT-PCR和免疫印迹结果显示，烟雾暴露后miR-155（-/-）小鼠的SOCS-1水平显著升高。此外，在分离的miR-155 KO肺中性粒细胞中进行的实验表明，在烟雾刺激下，缺乏SOCS-1会增强炎症细胞因子（MIP-2和KC）的分泌。综上所述，烟雾诱导miR-155的表达增加，miR-155通过抑制SOCS-1的表达参与了烟雾吸入诱导肺损伤的炎症反应。
Smoke inhalation causes acute lung injury (ALI), a severe clinical disease with high mortality. Accumulating evidence indicates that microRNA-155 (miR-155) and suppressor of cytokine signaling 1 (SOCS-1), as mediators of inflammatory response, are involved in the pathogenesis of ALI. In this paper, we explored the proinflammatory mechanism of miR-155 in smoke-inhalation-induced ALI. Our data revealed that smoke inhalation induces miR-155 expression, and miR-155 knockout (KO) significantly ameliorates smoke-inhalation-induced lung injury in mice. Neutrophil infiltration and myeloperoxidase (MPO), macrophage inflammatory protein 2 (MIP-2) and keratinocyte chemoattractant (KC) expressions were decreased in miR-155(-/-) mice after smoke inhalation as well. Real-time RT-PCR and immunoblotting results showed that SOCS-1 level was remarkably increased in miR-155(-/-) mice after smoke exposure. Furthermore, the experiments performed in isolated miR-155 KO pulmonary neutrophils demonstrated that the lack of SOCS-1 enhanced inflammatory cytokines (MIP-2 and KC) secretion in response to smoke stimulation. In conclusion, smoke induces increased expression of miR-155, and miR-155 is involved in inflammatory response to smoke-inhalation-induced lung injury by inhibiting the expression of SOCS-1.
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影响因子：
32.4
作者：
O'Connell RM;Kahn D;Gibson WS;Round JL;Scholz RL;Chaudhuri AA;Kahn ME;Rao DS;Baltimore D
通讯作者：
Baltimore D
DOI：
10.1126/science.1139253
发表时间：
2007-04-27
期刊：
Science (New York, N.Y.)
影响因子：
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DOI：
10.1152/ajplung.00384.2005
发表时间：
2006-07-01
影响因子：
4.9
作者：
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通讯作者：
Chung, Kian Fan
DOI：
10.1165/rcmb.2007-0287oc
发表时间：
2009-03-01
影响因子：
6.4
作者：
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影响因子：
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作者：
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