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脂肪来源干细胞条件培养基抑制侧流香烟烟雾提取物诱导的肺上皮细胞死亡和上皮-间充质转化。

Conditioned Media of Adipose-Derived Stem Cells Suppresses Sidestream Cigarette Smoke Extract Induced Cell Death and Epithelial-Mesenchymal Transition in Lung Epithelial Cells.

机构信息

Institute of Biomedical Engineering and Nanomedicine, National Health Research Institutes, Zhunan 35053, Taiwan.

Ditmanson Medical Foundation Chia-Yi Christian Hospital, Chia-Yi 600566, Taiwan.

出版信息

Int J Mol Sci. 2021 Nov 8;22(21):12069. doi: 10.3390/ijms222112069.

DOI:10.3390/ijms222112069
PMID:34769496
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8584490/
Abstract

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.

摘要

上皮-间充质转化 (EMT) 在肺上皮细胞中的作用正日益被认为是 COPD、纤维化和肺癌发展的关键阶段，这些疾病都与吸烟和二手烟暴露高度相关。本研究以人肺癌上皮 A549 细胞和非癌性 Beas-2B 细胞暴露于侧流香烟烟雾提取物 (CSE) 为模型，研究了脂肪干细胞条件培养基 (ADSC-CM) 对 CSE 诱导的细胞死亡和 EMT 的保护作用。CSE 呈剂量依赖性诱导细胞死亡，降低上皮标志物的表达，增加间充质标志物的表达。CSE 暴露后差异表达基因的上游调控分析显示，与 TGF-β1 诱导的典型 EMT 观察到的途径相似。ADSC-CM 明显减轻了 CSE 诱导的细胞死亡，但其他对照培养基（如 ADSC-CM 的穿透部分或 A549-CM）则没有。ADSC-CM 有效抑制了 CSE 诱导的 EMT，并能够逆转与 TGF-β1 处理相关的上皮标志物表达逐渐丧失。CSE 或 TGF-β1 使 A549 细胞的迁移速度增加了 2 到 3 倍，ADSC-CM 可有效阻断这两种因子诱导的细胞迁移。未来的工作将在这项体外研究的结果基础上，进一步确定 ADSC-CM 通过哪些分子机制来保护肺上皮细胞免受二手烟中有毒物质诱导的 EMT。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba5d/8584490/1af47545e9b4/ijms-22-12069-g006.jpg
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