LncRNA MALAT1 Participates in Protection of High-Molecular-Weight Hyaluronan against Smoke-Induced Acute Lung Injury by Upregulation of SOCS-1.
LncRNA MALAT1 Participates in Protection of High-Molecular-Weight Hyaluronan against Smoke-Induced Acute Lung Injury by Upregulation of SOCS-1.
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LncRNA MALAT1 通过上调 SOCS-1 参与保护高分子透明质酸免受烟雾引起的急性肺损伤
DOI：
10.3390/molecules27134128
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发表时间：
2022-06-27
期刊：
影响因子：
--
通讯作者：
中科院分区：
文献类型：
--
作者：
吸烟引起的急性肺损伤（Smoke-induced acute lung injury，ALI）是一种严重的疾病，病死率高。尽管医学干预取得了进展，但食品和药物管理局（FDA）尚未批准任何药物用于ALI。在这项研究中，我们报道了高分子量透明质酸（1600 kDa，HA 1600）的预处理减轻了暴露于烟雾的小鼠的肺部炎症和损伤，并上调了肺组织中长链非编码RNA（lncRNA）转移相关肺腺癌转录本1（MALAT 1）以及细胞因子信号传导抑制因子-1（SOCS-1）。接下来，我们通过气管内施用克隆有MALAT 1 cDNA的腺病毒在肺中过表达MALAT 1，并发现烟雾暴露后小鼠的存活率得到改善。此外，肺部MALAT 1过表达改善了小鼠烟雾诱导的ALI，并提高了肺部SOCS-1的水平。总之，结果表明，HA 1600通过增加MALAT 1水平和随后的SOCS-1表达而对烟雾诱导的ALI发挥保护作用。我们的研究提供了一种潜在的治疗方法，烟雾诱导的ALI和新的见解HA 1600的作用机制。
Smoke-induced acute lung injury (ALI) is a grievous disease with high mortality. Despite advances in medical intervention, no drug has yet been approved by the Food and Drug Administration (FDA) for ALI. In this study, we reported that pretreatment with high-molecular-weight hyaluronan (1600 kDa, HA1600) alleviated pulmonary inflammation and injury in mice exposed to smoke and also upregulated long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), as well as suppressor of cytokine signaling-1 (SOCS-1), in the lung tissues. Next, we overexpressed MALAT1 in the lungs by intratracheal administration of adenovirus cloned with MALAT1 cDNA and found that the survival of mice after smoke exposure was improved. Moreover, pulmonary overexpression of MALAT1 ameliorated smoke-induced ALI in mice and elevated the level of SOCS-1 in the lungs. In conclusion, the results pointed out that HA1600 exerted a protective effect against smoke-induced ALI through increasing the MALAT1 level and the subsequent SOCS-1 expression. Our study provides a potential therapeutic approach to smoke-induced ALI and a novel insight into the mechanism of action of HA1600.
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影响因子：
10.8
作者：
Miranda JJ;Bernabé-Ortiz A;Diez-Canseco F;Málaga G;Cárdenas MK;Carrillo-Larco RM;Lazo-Porras M;Moscoso-Porras M;Pesantes MA;Ponce V;Araya R;Beran D;Busse P;Boggio O;Checkley W;García PJ;Huicho L;León-Velarde F;Lescano AG;Mohr DC;Pan W;Peiris D;Perel P;Rabadán-Diehl C;Rivera-Chira M;Sacksteder K;Smeeth L;Trujillo AJ;Wells JC;Yan LL;García HH;Gilman RH
通讯作者：
Gilman RH
DOI：
10.1186/cc6982
发表时间：
2008
期刊：
Critical care (London, England)
影响因子：
--
作者：
Liu YY;Lee CH;Dedaj R;Zhao H;Mrabat H;Sheidlin A;Syrkina O;Huang PM;Garg HG;Hales CA;Quinn DA
通讯作者：
Quinn DA
DOI：
10.1016/j.numecd.2018.06.017
发表时间：
2018-11-01
影响因子：
3.9
作者：
Li, S.;Sun, Y.;Chen, X.
通讯作者：
Chen, X.
DOI：
10.1164/rccm.202009-3536oc
发表时间：
2021-06-01
影响因子：
24.7
作者：
Goligher, Ewan C.;Costa, Eduardo L., V;Amato, Marcelo P. B.
通讯作者：
Amato, Marcelo P. B.
长非编码RNA MALAT1通过抑制细胞凋亡保护支气管肺发育不良早产儿
影响因子：
3.1
作者：
Cai, Cheng;Qiu, Jiajun;Gong, Xiaohui
通讯作者：
Gong, Xiaohui