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CD147 通过氧化应激信号通路促进香烟烟雾诱导的气道上皮细胞上皮间质转化。

CD147 Promoted Epithelial Mesenchymal Transition in Airway Epithelial Cells Induced by Cigarette Smoke via Oxidative Stress Signaling Pathway.

机构信息

Department of Respiratory Medicine, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, Zhejiang, P.R. China.

Key Laboratory of Tumor Molecular Diagnosis and Individualized Medicine of Zhejiang Province, Hangzhou, Zhejiang, P.R. China.

出版信息

COPD. 2020 Jun;17(3):269-279. doi: 10.1080/15412555.2020.1758051. Epub 2020 May 5.

Abstract

Chronic obstructive pulmonary disease (COPD) is a common airway disease, and epithelial mesenchymal transition (EMT) is participated in the pathogenesis of COPD. However, the role of CD147 in COPD remains largely unknown. In order to clarify the role of CD147 in EMT induced by cigarette smoke, we established animal and cell model of EMT by mean of cigarette smoke exposure and detected the expressions of CD147 and EMT markers PCR, WB and IF. RNA inference was applied to study the role of CD147 in CSE induced EMT . NAC and HO were used to study oxidative stress signaling pathway in this model. As a result, cigarette smoke exposure upregulated the expressions of CD147, α-SMA, and Vimentin and downregulated the expression of Ecadherin and ZO1 both and , which was accompanied by augmented level of oxidative stress. CD147 knockdown would partly inhibit CSE induced EMT, while preincubation of HO could inverse this effect. In conclusion, CD147 promoted EMT in mice and HBE cells induced by cigarette smoke oxidative stress signaling pathway.

摘要

慢性阻塞性肺疾病(COPD)是一种常见的气道疾病,上皮间质转化(EMT)参与了 COPD 的发病机制。然而,CD147 在 COPD 中的作用在很大程度上仍然未知。为了阐明 CD147 在香烟烟雾诱导的 EMT 中的作用,我们通过香烟烟雾暴露建立了 EMT 的动物和细胞模型,并通过 PCR、WB 和 IF 检测 CD147 和 EMT 标志物的表达。RNA 干扰用于研究 CD147 在 CSE 诱导的 EMT 中的作用。NAC 和 HO 用于研究该模型中的氧化应激信号通路。结果表明,香烟烟雾暴露上调了 CD147、α-SMA 和波形蛋白的表达,下调了 Ecadherin 和 ZO1 的表达,同时伴有氧化应激水平的升高。CD147 敲低部分抑制了 CSE 诱导的 EMT,而 HO 的预孵育可以逆转这种作用。总之,CD147 通过氧化应激信号通路促进香烟烟雾诱导的小鼠和 HBE 细胞 EMT。

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