Long non-coding RNA CASC2 improved acute lung injury by regulating miR-144-3p/AQP1 axis to reduce lung epithelial cell apoptosis.
Long non-coding RNA CASC2 improved acute lung injury by regulating miR-144-3p/AQP1 axis to reduce lung epithelial cell apoptosis.
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DOI：
10.1186/s13578-018-0205-7
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发表时间：
2018
影响因子：
7.5
通讯作者：
Sun R
中科院分区：
文献类型：
--
作者：
Li H;Shi H;Gao M;Ma N;Sun R
肺上皮细胞凋亡与急性肺损伤（ALI）的发病机制有关。探讨癌易感候选物2（CASC2）对LPS诱导小鼠急性肺损伤后减少肺上皮细胞凋亡的保护作用及机制。通过气管内滴注脂多糖(LPS)建立ALI小鼠模型。通过实时定量聚合酶链反应检测到的CASC2表达在LPS诱导的A549细胞和ALI小鼠模型中显着降低。 LPS诱导A549细胞凋亡，而pcDNA-CASC2转染则逆转了增加的细胞凋亡，表明CASC2的过表达抑制了LPS诱导的A549细胞凋亡。此外，我们发现在LPS诱导的A549细胞和ALI小鼠模型中，miR-144-3p表达与CASC2相反，而Aquaporin-1（AQP1）表达与miR-144-3p相反。 RNA 免疫沉淀和 RNA Pull-down 测定表明 CASC2 可以充当 miR-144-3p 诱饵。荧光素酶报告基因检测显示 AQP1 是 A549 细胞中 miR-144-3p 的靶标。然后，进一步的体外研究表明，CASC2通过调节miR-144-3p来控制AQP1的表达，而LPS通过调节CASC2/miR-144-3p/AQP1轴来诱导A549细胞凋亡。最后，注射表达慢病毒的CASC2或对照慢病毒后，气管内滴注LPS。与注射pcDNA的小鼠相比，注射pcDNA-CASC2的小鼠的肺湿干重比显着降低。长非编码RNA CASC2通过调节miR-144-3p/AQP1轴减少肺上皮细胞凋亡来改善急性肺损伤。
Apoptosis of lung epithelial cell is implicated in the pathogenesis of acute lung injury (ALI). To study the protective effect and mechanism of cancer susceptibility candidate 2 (CASC2) on reducing lung epithelial cell apoptosis after LPS inducing acute lung injury in mice. The ALI mice model was performed by intratracheally instilling with lipopolysaccharide (LPS). The CASC2 expression detected by quantitative real-time polymerase chain reaction was significantly decreased in LPS-induced A549 cell and ALI mice model. LPS induced A549 cell apoptosis, while transfection with pcDNA-CASC2 reversed the increased cell apoptosis, suggesting overexpression of CASC2 inhibited LPS-induced A549 cell apoptosis. In addition, we found that miR-144-3p expression were opposite to CASC2, while Aquaporin-1 (AQP1) expression was opposite to miR-144-3p in LPS-induced A549 cell and ALI mice model. The RNA immunoprecipitation and RNA pull-down assay demonstrated that CASC2 could function as a miR-144-3p decoy. The luciferase reporter assay revealed that AQP1 was a target of miR-144-3p in A549 cell. And then, further in vitro studied showed that CASC2 controlled AQP1 expression by regulating miR-144-3p, and LPS induced A549 cell apoptosis by regulating CASC2/miR-144-3p/AQP1 axis. At last, after injection with lentivirus-expressing CASC2 or control lentivirus, the mice were intratracheally instilled with LPS. Comparing to the mice injected with pcDNA, the mice injected with pcDNA-CASC2 had a significantly reduced lung wet–dry weight ratio. Long non-coding RNA CASC2 improved acute lung injury by regulating miR-144-3p/AQP1 axis to reduce lung epithelial cell apoptosis.
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影响因子：
--
作者：
Wu C;Xu B;Zhou Y;Ji M;Zhang D;Jiang J;Wu C
通讯作者：
Wu C
影响因子：
4.6
作者：
Huang G;Wu X;Li S;Xu X;Zhu H;Chen X
通讯作者：
Chen X
影响因子：
2.7
作者：
Fan M;Li X;Jiang W;Huang Y;Li J;Wang Z
通讯作者：
Wang Z
影响因子：
5.6
作者：
Tao, Weiwei;Su, Qiang;Wang, Shumin
通讯作者：
Wang, Shumin
DOI：
10.1016/j.trsl.2011.01.010
发表时间：
2011-04
期刊：
Translational research : the journal of laboratory and clinical medicine
影响因子：
--
作者：
Zhou T;Garcia JG;Zhang W
通讯作者：
Zhang W