JAK2/STAT3 Pathway Was Associated with the Protective Effects of IL-22 On Aortic Dissection with Acute Lung Injury.
JAK2/STAT3 Pathway Was Associated with the Protective Effects of IL-22 On Aortic Dissection with Acute Lung Injury.
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JAK2/STAT3 通路与 IL-22 对主动脉夹层急性肺损伤的保护作用相关
DOI：
10.1155/2017/1917804
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发表时间：
2017
期刊：
影响因子：
--
通讯作者：
Ruan Y
中科院分区：
文献类型：
--
作者：
Ren W;Wang Z;Wu Z;Hu Z;Dai F;Chang J;Li B;Liu H;Ruan Y
主动脉夹层（AD）患者可出现急性肺损伤（ALI），影响预后。本研究旨在探讨IL-22在AD合并ALI发病中的作用及其机制。分析621例AD患者的ALI发生率和肺部CT表现。通过AngII建立小鼠ALI模型，然后注射IL-22和给予AG490。观察病理改变、炎性细胞浸润及STAT3的表达。对于体外实验，培养的肺微血管内皮细胞（PMVEC）用血管紧张素II（AngII）处理，然后用IL-22和/或AG490处理。测定STAT3的表达和迁移。流式细胞仪检测细胞凋亡情况。IL-22可促进肺组织STAT3的表达，减轻ALI。IL-22可明显抑制AngII介导的PMVECs凋亡，下调STAT3的表达和核内传递。这种现象在给予JAK 2的抑制剂AG490后被完全抑制。IL-22可能通过激活JAK2/STAT3信号通路抑制AngII介导的PMVEC凋亡，从而减轻AngII诱导的ALI。
Patients with aortic dissection (AD) may present acute lung injury (ALI) that may affect the prognosis. In this study, we aim to investigate the roles and mechanism of IL-22 in the pathogenesis of AD complicated with ALI. Six hundred and twenty-one AD patients were included, and the incidence of ALI and pulmonary CT findings were analyzed. Mouse ALI model was established through AngII, and then IL-22 injection and AG490 were given. The pathological changes, infiltration of inflammatory cells, and expression of STAT3 were determined. For the in vitro experiment, cultivated pulmonary microvascular endothelial cells (PMVECs) were treated by angiotensin II (AngII), followed by treating with IL-22 and/or AG490. The expression and migration of STAT3 was determined. Flow cytometry was carried out to evaluate the apoptosis. IL-22 contributed to the expression of STAT3 in lung tissues and attenuation of ALI. IL-22 obviously inhibited the apoptosis of PMVECs mediated by AngII and downregulated the expression and intranuclear transmission of STAT3. Such phenomenon was completely inhibited upon administration of AG490, an inhibitor of JAK2. Our data showed IL-22 contributed to the inhibition of PMVEC apoptosis mediated by AngII through activating the JAK2/STAT3 signaling pathway, which may attenuate the ALI induced by AngII.
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DOI：
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发表时间：
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影响因子：
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作者：
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Modesti, Pietro Amedeo
影响因子：
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作者：
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影响因子：
4.9
作者：
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