Overexpression of MECP2 attenuates cigarette smoke extracts induced lung epithelial cell injury by promoting CYP1B1 methylation
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- Lin Junhong
- Neonatology department, the First Affiliated Hospital, Jinan University, China
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- Peng Junzheng
- Department of Respiration, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, China
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- Liu Guosheng
- Neonatology department, the First Affiliated Hospital, Jinan University, China
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- Deng Li
- Department of Respiration, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, China
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<p>MECP2 (Methyl-CpG-binding protein 2) has been shown to have a critical role in regulating DNA methylation against smoke exposed lung injury. However, the biological function of MECP2 and the underlying molecular mechanism remains elusive. Human bronchial epithelial (16HBE) and alveolar type II epithelial cells (AECII) were exposed to increasing concentrations of cigarette smoke extracts (CSE) solution to establish CSE-induced lung epithelial cell injury models. Our findings revealed that MECP2 was down-regulated, while CYP1B1 was up-regulated in CSE-induced lung epithelial cell injury models by quantitative real time PCR, western blotting and immunofluorescence staining. Down-regulated CYP1B1 was ascribed to the demethylation of its promoter by methylation-specific PCR (MSP). The in vitro experiments further showed that MECP2 overexpression significantly attenuated CSE-triggered cell growth attenuation, cell cycle arrest, apoptosis and ROS generation in lung epithelial cells by CCK-8 and flow cytometry assays. In molecular level, we further demonstrated that MECP2 overexpression obviously suppressed the expression of CYP1B1 through enhancing DNA methylation. Therefore, our data suggest that MECP2 protects against CSE-induced lung epithelial cell injury possibly through down-regulating CYP1B1 expression via elevating its methylation status.</p>
収録刊行物
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- The Journal of Toxicological Sciences
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The Journal of Toxicological Sciences 45 (3), 177-186, 2020
一般社団法人 日本毒性学会
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詳細情報 詳細情報について
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- CRID
- 1390002184880323584
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- NII論文ID
- 130007806339
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- NII書誌ID
- AN00002808
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- ISSN
- 18803989
- 03881350
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- NDL書誌ID
- 030384517
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- PubMed
- 32147640
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 使用不可