In Vivo Disruption of TGF-(beta) Signaling by Smad7 in Airway Epithelium Alleviates Allergic Asthma but Aggravates Lung Carcinogenesis in Mouse
文献类型：期刊论文
| 作者 | Luo, Xiaolin; Ding, QiuRong（丁秋蓉） ; Wang, Min; Li, Zhigang; Mao, Kairui; Sun, Bing; Pan, Yi（潘怡）; Wang, ZhenZhen（王甄真）; Zang, Ying Qin; Chen, Yan（陈雁）
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| 刊名 | PLOS ONE
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| 出版日期 | 2010 |
| 卷号 | 5期号:4页码:0 |
| 英文摘要 | Background: TGF-beta has been postulated to play an important role in the maintenance of epithelial homeostasis and the development of epithelium-derived cancers. However, most of previous studies are mainly focused on the function of TGF-beta in immune cells to the development of allergic asthma and how TGF-beta signaling in airway epithelium itself in allergic inflammation is largely unknown. Furthermore, the in vivo TGF-beta function specifically in the airway epithelium during lung cancer development has been largely elusive. Methodology/Principal Findings: To evaluate the in vivo contribution of TGF-beta signaling in lung epithelium to the development of allergic disease and lung cancer, we generated a transgenic mouse model with Smad7, an intracellular inhibitor of TGF-beta signaling, constitutively expressed in mouse airway Clara cells using a mouse CC10 promoter. The mice were subjected to the development of OVA-induced allergic asthma and urethane-induced lung cancer. The Smad7 transgenic animals significantly protected from OVA-induced asthma, with reduced airway inflammation, airway mucus production, extracellular matrix deposition, and production of OVA-specific IgE. Further analysis of cytokine profiles in lung homogenates revealed that the Th2 cytokines including IL-4, IL-5 and IL-13, as well as other cytokines including IL-17, IL-1, IL-6, IP10, G-CSF, and GM-CSF were significantly reduced in the transgenic mice upon OVA induction. In contrast, the Smad7 transgenic animals had an increased incidence of lung carcinogenesis when subjected to urethane treatment. Conclusion/Significance: These studies, therefore, demonstrate for the first time the in vivo function of TGF-beta signaling specifically in airway epithelium during the development of allergic asthma and lung cancer. |
| 类目[WOS] | Multidisciplinary Sciences |
| 关键词[WOS] | COLONY-STIMULATING FACTOR ; TGF-BETA ; T-CELLS ; INFLAMMATION ; CANCER ; MACROPHAGE ; EXPRESSION ; RECEPTOR ; HYPERRESPONSIVENESS ; INTERLEUKIN-10 |
| 收录类别 | SCI |
| 语种 | 英语 |
| WOS记录号 | WOS:000276706300006 |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.144/handle/331004/82]  |
| 专题 | 中国科学院上海生命科学研究院营养科学研究所_信号转导与营养相关疾病研究组 |
| 推荐引用方式 GB/T 7714 | Luo, Xiaolin,Ding, QiuRong,Wang, Min,et al. In Vivo Disruption of TGF-(beta) Signaling by Smad7 in Airway Epithelium Alleviates Allergic Asthma but Aggravates Lung Carcinogenesis in Mouse[J]. PLOS ONE,2010,5(4):0. |
| APA | Luo, Xiaolin.,Ding, QiuRong.,Wang, Min.,Li, Zhigang.,Mao, Kairui.,...&Chen, Yan.(2010).In Vivo Disruption of TGF-(beta) Signaling by Smad7 in Airway Epithelium Alleviates Allergic Asthma but Aggravates Lung Carcinogenesis in Mouse.PLOS ONE,5(4),0. |
| MLA | Luo, Xiaolin,et al."In Vivo Disruption of TGF-(beta) Signaling by Smad7 in Airway Epithelium Alleviates Allergic Asthma but Aggravates Lung Carcinogenesis in Mouse".PLOS ONE 5.4(2010):0. |
入库方式： OAI收割
来源：上海营养与健康研究所
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