دورية أكاديمية

Multiwalled Carbon Nanotubes Induce Fibrosis and Telomere Length Alterations

التفاصيل البيبلوغرافية
العنوان: Multiwalled Carbon Nanotubes Induce Fibrosis and Telomere Length Alterations
المؤلفون: Mayes Alswady-Hoff, Johanna Samulin Erdem, Mona Aleksandersen, Kristine Haugen Anmarkrud, Øivind Skare, Fang-Chin Lin, Vincent Simensen, Yke Jildouw Arnoldussen, Vidar Skaug, Erik Ropstad, Shanbeh Zienolddiny-Narui
المصدر: International Journal of Molecular Sciences, Vol 23, Iss 11, p 6005 (2022)
بيانات النشر: MDPI AG, 2022.
سنة النشر: 2022
المجموعة: LCC:Biology (General)
LCC:Chemistry
مصطلحات موضوعية: manufactured nanomaterials, MWCNT, telomere instability, long-term exposure, inflammation, fibrosis, Biology (General), QH301-705.5, Chemistry, QD1-999
الوصف: Telomere shortening can result in cellular senescence and in increased level of genome instability, which are key events in numerous of cancer types. Despite this, few studies have focused on the effect of nanomaterial exposure on telomere length as a possible mechanism involved in nanomaterial-induced carcinogenesis. In this study, effects of exposure to multiwalled carbon nanotubes (MWCNT) on telomere length were investigated in mice exposed by intrapleural injection, as well as in human lung epithelial and mesothelial cell lines. In addition, cell cycle, apoptosis, and regulation of genes involved in DNA damage repair were assessed. Exposure to MWCNT led to severe fibrosis, infiltration of inflammatory cells in pleura, and mesothelial cell hyperplasia. These histological alterations were accompanied by deregulation of genes involved in fibrosis and immune cell recruitment, as well as a significant shortening of telomeres in the pleura and the lung. Assessment of key carcinogenic mechanisms in vitro confirmed that long-term exposure to the long MWCNT led to a prominent telomere shortening in epithelial cells, which coincided with G1-phase arrest and enhanced apoptosis. Altogether, our data show that telomere shortening resulting in cell cycle arrest and apoptosis may be an important mechanism in long MWCNT-induced inflammation and fibrosis.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 23116005
1422-0067
1661-6596
Relation: https://www.mdpi.com/1422-0067/23/11/6005; https://doaj.org/toc/1661-6596; https://doaj.org/toc/1422-0067
DOI: 10.3390/ijms23116005
URL الوصول: https://doaj.org/article/29b491e4149645b5abe2b0d572d73aa3
رقم الأكسشن: edsdoj.29b491e4149645b5abe2b0d572d73aa3
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:23116005
14220067
16616596
DOI:10.3390/ijms23116005