Conditioned Media of Adipose-Derived Stem Cells Suppresses Sidestream Cigarette Smoke Extract Induced Cell Death and Epithelial-Mesenchymal Transition in Lung Epithelial Cells.
Conditioned Media of Adipose-Derived Stem Cells Suppresses Sidestream Cigarette Smoke Extract Induced Cell Death and Epithelial-Mesenchymal Transition in Lung Epithelial Cells.
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DOI：
10.3390/ijms222112069
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发表时间：
2021-11-08
影响因子：
5.6
通讯作者：
Lin KM
中科院分区：
文献类型：
--
作者：
Chen TY;Liu CH;Chen TH;Chen MR;Liu SW;Lin P;Lin KM
肺上皮细胞中上皮-间质转化（EMT）的作用越来越被认为是COPD、纤维化和肺癌发展的关键阶段，这些疾病都与吸烟和暴露于二手烟高度相关。以香烟烟雾提取物（CSE）诱导的人肺癌A549细胞和非癌Beas-2B细胞凋亡为模型，研究了脂肪干细胞条件培养液（ADSC-CM）对CSE诱导的细胞死亡和EMT的保护作用。CSE剂量依赖性地诱导细胞死亡，减少上皮标志物，并增加间充质标志物的表达。对CSE暴露后差异表达基因的上游调控因子分析显示，与TGF-β1诱导的典型EMT中观察到的途径相似。CSE诱导的细胞死亡被ADSC-CM明显减弱，但不被其他对照培养基，如ADSC-CM或A549-CM的通过级分。ADSC-CM有效抑制CSE诱导的EMT，并能够逆转与TGF-β1治疗相关的上皮标志物表达的逐渐丧失。CSE或TGF-β1可使A549细胞迁移速度提高2 ~ 3倍，ADSC-CM可有效阻断CSE或TGF-β1诱导的细胞迁移。未来的工作将建立在这项体外研究的结果，通过定义ADSC-CM保护肺上皮细胞免受二手烟中有毒物质诱导的EMT的分子机制。
The role of the epithelial–mesenchymal transition (EMT) in lung epithelial cells is increasingly being recognized as a key stage in the development of COPD, fibrosis, and lung cancers, which are all highly associated with cigarette smoking and with exposure to second-hand smoke. Using the exposure of human lung cancer epithelial A549 cells and non-cancerous Beas-2B cells to sidestream cigarette smoke extract (CSE) as a model, we studied the protective effects of adipose-derived stem cell-conditioned medium (ADSC-CM) against CSE-induced cell death and EMT. CSE dose-dependently induced cell death, decreased epithelial markers, and increased the expression of mesenchymal markers. Upstream regulator analysis of differentially expressed genes after CSE exposure revealed similar pathways as those observed in typical EMT induced by TGF-β1. CSE-induced cell death was clearly attenuated by ADSC-CM but not by other control media, such as a pass-through fraction of ADSC-CM or A549-CM. ADSC-CM effectively inhibited CSE-induced EMT and was able to reverse the gradual loss of epithelial marker expression associated with TGF-β1 treatment. CSE or TGF-β1 enhanced the speed of A549 migration by 2- to 3-fold, and ADSC-CM was effective in blocking the cell migration induced by either agent. Future work will build on the results of this in vitro study by defining the molecular mechanisms through which ADSC-CM protects lung epithelial cells from EMT induced by toxicants in second-hand smoke.
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DOI：
10.1152/ajplung.00253.2010
发表时间：
2011-09-01
影响因子：
4.9
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影响因子：
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