{"title":"Function and Potential ceRNA Identification of Circ_009773 in Neodymium Oxide Nanoparticle-Induced Lung Epithelial Mesenchymal Transition.","authors":"Lei Gao, Juan Juan, Zimeng Zheng, Lihua Huang","doi":"10.3390/toxics12120917","DOIUrl":null,"url":null,"abstract":"<p><p>Nanoparticles of neodymium oxide (NPs-Nd<sub>2</sub>O<sub>3</sub>) can induce respiratory-related diseases, including lung tissue injury when entering the organism through the respiratory tract. However, it is currently unclear whether they can induce epithelial-mesenchymal transition (EMT) in lung tissue and the related mechanisms. In this study, we investigated the function of circ_009773 in the process of EMT induced by NPs-Nd<sub>2</sub>O<sub>3</sub> in lung tissue from in vivo as well as in vitro experiments. The findings showed that NPs-Nd<sub>2</sub>O<sub>3</sub> induced EMT in 16HBE cells and SD rat lung tissues. This was characterised by a decrease in epithelial markers and an increase in mesenchymal markers. Additionally, circ_009773 expression was found to decrease in 16HBE cells infected with NPs-Nd<sub>2</sub>O<sub>3</sub> and also decreased in the lung tissues of SD rats. Relevant experiments showed that circ_009773 inhibited EMT in NPs-Nd<sub>2</sub>O<sub>3</sub>-treated 16HBE cells and SD rat lung tissues. The previous experiments revealed that circ_009773 was localised in the cytoplasm and functioned at the post-transcriptional level. With the EMT-related pathway used as the basis for circ_009773-related competing endogenous (ce)RNA mechanisms, our observations indicate that circ_009773 is capable of binding to and regulating the expression of miR-135b-5p. In summary, we found that circ_009773 inhibits the EMT induced by NPs-Nd<sub>2</sub>O<sub>3</sub> in lung tissues, and this process likely occurs through competitive binding to miR-135b-5p.</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"12 12","pages":""},"PeriodicalIF":3.9000,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11728544/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Toxics","FirstCategoryId":"93","ListUrlMain":"https://doi.org/10.3390/toxics12120917","RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ENVIRONMENTAL SCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
Nanoparticles of neodymium oxide (NPs-Nd2O3) can induce respiratory-related diseases, including lung tissue injury when entering the organism through the respiratory tract. However, it is currently unclear whether they can induce epithelial-mesenchymal transition (EMT) in lung tissue and the related mechanisms. In this study, we investigated the function of circ_009773 in the process of EMT induced by NPs-Nd2O3 in lung tissue from in vivo as well as in vitro experiments. The findings showed that NPs-Nd2O3 induced EMT in 16HBE cells and SD rat lung tissues. This was characterised by a decrease in epithelial markers and an increase in mesenchymal markers. Additionally, circ_009773 expression was found to decrease in 16HBE cells infected with NPs-Nd2O3 and also decreased in the lung tissues of SD rats. Relevant experiments showed that circ_009773 inhibited EMT in NPs-Nd2O3-treated 16HBE cells and SD rat lung tissues. The previous experiments revealed that circ_009773 was localised in the cytoplasm and functioned at the post-transcriptional level. With the EMT-related pathway used as the basis for circ_009773-related competing endogenous (ce)RNA mechanisms, our observations indicate that circ_009773 is capable of binding to and regulating the expression of miR-135b-5p. In summary, we found that circ_009773 inhibits the EMT induced by NPs-Nd2O3 in lung tissues, and this process likely occurs through competitive binding to miR-135b-5p.
ToxicsChemical Engineering-Chemical Health and Safety
CiteScore
4.50
自引率
10.90%
发文量
681
审稿时长
6 weeks
期刊介绍:
Toxics (ISSN 2305-6304) is an international, peer-reviewed, open access journal which provides an advanced forum for studies related to all aspects of toxic chemicals and materials. It publishes reviews, regular research papers, and short communications. Our aim is to encourage scientists to publish their experimental and theoretical results in detail. There is, therefore, no restriction on the maximum length of the papers, although authors should write their papers in a clear and concise way. The full experimental details must be provided so that the results can be reproduced. Electronic files or software regarding the full details of calculations and experimental procedure can be deposited as supplementary material, if it is not possible to publish them along with the text.