Dynamic assessing silica particle-induced pulmonary fibrosis and associated regulation of long non-coding RNA expression in Wistar rats

Linlin Sai,Qiang Jia,Xuejie Qi,Yuxin Zheng,Cheng Peng,Juan Zhang,Gongchang Yu

doi:10.1186/s41021-021-00193-3

Abstract

BackgroundExposure to respirable crystalline silica (RCS) can induce accelerated silicosis (AS), a form of silicosis that is more progressive and severe form of silicosis. In this project we aimed to assess processes of silicosis in rats exposed to RCS with focus on the regulation of long noncoding RNAs (lncRNAs).ResultsThe results showed that RCS induced acute inflammatory response as indicated by the appearance of inflammatory cells in the lung from the first day and peaked on day 7 of exposure. The fibroblasts appeared along with the inflammatory cells decreasing gradually on day 14. Extensive fibrosis appeared in the lung tissue, and silicon nodules were getting larger on day 28. Interestingly, the number of altered lncRNAs increased with the exposure time with 193, 424, 455, 421 and 682 lncRNAs on day 1, 7, 14, 21, and 28 after exposure, respectively. We obtained 285 lncRNAs with five significant temporal expression patterns whose expressions might correlate with severity of silicosis. KEGG analysis showed that lncRNAs from short time-series expression miner (STEM)-derived data mainly involved in 17 pathways such as complement and coagulation cascades.ConclusionsThe differential expression profiles of lncRNAs may be potential biomarkers in silicosis through modulating expressions of their relevant genes in lungs of rat and thus warrant further investigation.

Highlights

Silicosis is an irreversible lung disease with pulmonary diffuse fibrosis as main manifestation resulting from long-term inhalation of occupational dust containing silica particles [1]
Our results showed that rats exposed to silicon dioxide by disposable intratracheally instilled method were induced inflammation and pulmonary fibrosis from 1 to 28 days after exposure
The change of the number of differentially expressed long noncoding RNAs (lncRNAs) may be related to the progression of pulmonary inflammation and fibrosis in rats

Summary

Introduction

Silicosis is an irreversible lung disease with pulmonary diffuse fibrosis as main manifestation resulting from long-term inhalation of occupational dust containing silica particles [1]. The molecular mechanism of silicosis, especially AS has not been clearly understood yet, which hindered the effective treatment and prevention. This highlights the urgent need to explore the early response to RCS at different levels in initiation and key factors in progression and development of silicosis to identify the possible reliable biomarkers for early diagnosis or monitoring disease status. Exposure to respirable crystalline silica (RCS) can induce accelerated silicosis (AS), a form of silicosis that is more progressive and severe form of silicosis In this project we aimed to assess processes of silicosis in rats exposed to RCS with focus on the regulation of long noncoding RNAs (lncRNAs)

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Discussion

Conclusion