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. 2019 Jan 24;9:471. doi: 10.1038/s41598-018-36712-6

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Schematic diagram of the initiation of pulmonary fibrosis after silica inhalation is associated with shelterin dysregulation and dsDNA break in rat lung that may lead to a persistent and severe DDR (TTI2) at telomeres characterized by increased γH2AX and αSMA. Silica inhalation caused an increased staining in the number of γH2AX positive cells and an elevated αSMA expression in lung tissue compared to air control. Initiation of shelterin dysregulation was started after 3 wk of silica exposure as shown by the disruption of Tin2-TPP1 and remained persistent at 6 and 12 wk of silica exposure.