C-EBPβ mediates in cigarette/IL-17A-induced bronchial epithelial-mesenchymal transition in COPD mice.
C-EBPβ mediates in cigarette/IL-17A-induced bronchial epithelial-mesenchymal transition in COPD mice.
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DOI：
10.1186/s12890-021-01738-6
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发表时间：
2021-11-18
影响因子：
3.1
通讯作者：
Pan Q
中科院分区：
文献类型：
--
作者：
Chu S;Ma L;Wu Y;Zhao X;Xiao B;Pan Q
吸烟和IL-17A会导致慢性阻塞性肺疾病（COPD），并对支气管上皮细胞增殖产生协同作用。 CCAAT/增强子结合蛋白 β (C-EBPβ) 可由 IL-17A 诱导，并在 COPD 中上调。在本研究中，我们探讨了香烟和 IL-17 对 COPD 小鼠支气管上皮间质转化 (EMT) 的影响以及与 C-EBPβ 相关的潜在机制。通过小鼠吸烟建立COPD模型。在肺组织中检测到 E-钙粘蛋白、波形蛋白、IL-17A 和 C-EBPβ 分布。从健康小鼠中分离出原代支气管上皮细胞，并与香烟烟雾提取物（CSE）或/和IL-17A共培养。评估了 E-钙粘蛋白、波形蛋白和 IL-17 受体 (IL-17R) 的体外表达。当细胞中的C-EBPβ被siRNA沉默时，可检测到E-Cadherin、Vimentin和C-EBPβ的表达。与对照组相比，COPD 小鼠支气管中 E-Cadherin 分布较少，Vimentin 分布较多。 COPD小鼠肺组织中IL-17A和C-EBPβ的表达高于对照组。体外实验中，CSE + IL-17A组C-EBPβ蛋白表达量最高，其次是CSE和IL-17A组。 CSE + IL-17A组体外E-cadherin表达最低，Vimentin表达最高，其次是CSE或IL-17A组。这些可以被 C-EBPβ 沉默所抑制。 C-EBPβ 介导 COPD 小鼠中香烟/IL-17A 诱导的支气管 EMT。我们的研究结果有助于更好地了解从慢性阻塞性肺病到肺癌的进展，这将为预防吸烟背景下气道肿瘤的发生提供新途径。
Cigarettes smoking and IL-17A contribute to chronic obstructive pulmonary disease (COPD), and have synergistical effect on bronchial epithelial cell proliferation. CCAAT/enhancer-binding protein β (C-EBPβ) could be induced by IL-17A and is up-regulated in COPD. We explored the effect of cigarettes and IL-17 on bronchial epithelial–mesenchymal transition (EMT) in COPD mice and potential mechanism involved with C-EBPβ in this study. COPD model was established with mice by exposing to cigarettes. E-Cadherin, Vimentin, IL-17A and C-EBPβ distributions were detected in lung tissues. Primary bronchial epithelial cells were separated from health mice and cocultured with cigarette smoke extract (CSE) or/and IL-17A. E-Cadherin, Vimentin and IL-17 receptor (IL-17R) expressions in vitro were assessed. When C-EBPβ were silenced by siRNA in cells, E-Cadherin, Vimentin and C-EBPβ expressions were detected. E-Cadherin distribution was less and Vimentin distribution was more in bronchus of COPD mice than controls. IL-17A and C-EBPβ expressions were higher in lung tissues of COPD mice than controls. In vitro, C-EBPβ protein expression was highest in CSE + IL-17A group, followed by CSE and IL-17A groups. E-cadherin expression in vitro was lowest and Vimentin expression was highest in CSE + IL-17A group, followed by CSE or IL-17A group. Those could be inhibited by C-EBPβ silenced. C-EBPβ mediates in cigarette/IL-17A-induced bronchial EMT in COPD mice. Our findings contribute to a better understanding on the progress from COPD to lung cancers, which will provide novel avenues in preventing tumorigenesis of airway in the context of cigarette smoking.
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影响因子：
5.6
作者：
Ou SC;Bai KJ;Cheng WH;Chen JY;Lin CH;Wen HC;Chen BC
通讯作者：
Chen BC
影响因子：
4.8
作者：
Caivano, M;Gorgoni, B;Poli, V
通讯作者：
Poli, V
上皮间质转变相关蛋白的表达及其在肺腺癌中的临床意义。
影响因子：
2.6
作者：
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通讯作者：
Fan X
影响因子：
15.9
作者：
Salazar, Ylia;Zheng, Xiang;Savai, Rajkumar
通讯作者：
Savai, Rajkumar
影响因子：
3.8
作者：
Montalbano, Angela Marina;Riccobono, Loredana;Profita, Mirella
通讯作者：
Profita, Mirella