Abstract
Pulmonary fibrosis is a kind of interstitial lung disease with architectural remodeling of tissues and excessive matrix deposition. Apart from messenger RNA (mRNA), microRNA (miRNA), long non-coding RNA (lncRNA), and circular RNA (circRNA) could also play important roles in the regulatory processes of occurrence and progression of pulmonary fibrosis. In the present study, the pulmonary fibrosis model was administered with bleomycin. Whole transcriptome sequencing analysis was applied to investigate the expression profiles of mRNAs, lncRNAs, circRNAs, and miRNAs. After comparing bleomycin-induced pulmonary fibrosis model lung samples and controls, 286 lncRNAs, 192 mRNAs, 605 circRNAs, and 32 miRNAs were found to be differentially expressed. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to investigate the potential functions of these differentially expressed (DE) mRNAs and non-coding RNAs (ncRNAs). The terms related to inflammatory response and tumor necrosis factor (TNF) signaling pathway were enriched, implying potential roles in regulatory process. In addition, two co-expression networks were also constructed to understand the internal regulating relationships of these mRNAs and ncRNAs. Our study provides a systematic perspective on the potential functions of these DE mRNAs and ncRNAs during PF process and could help pave the way for effective therapeutics for this devastating and complex disease.
Highlights
Pulmonary fibrosis is a kind of lung disease that is a progressive and life-threatening pathologic process resulting in organ failure
Masson staining was applied to identify whether the pulmonary fibrosis rat model was successfully established
All the features mentioned above indicated that pulmonary fibrosis rat model had been successfully established
Summary
Pulmonary fibrosis is a kind of lung disease that is a progressive and life-threatening pathologic process resulting in organ failure. This fibroproliferative disease resulted from a various group of lung disorders with similar clinical, pathophysiologic, and radiographic characteristics and are known as interstitial lung disease (Pardo and Selman, 2002). The wound-healing response of pulmonary fibrotic conditions can be classified into three distinct phases: injury, inflammation, and repair (Wilson and Wynn, 2009). Many key genes, such as transforming growth factor beta (TGF-β), interleukin (IL) gene family members, vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), are involved in the wound-healing response of pulmonary fibrotic condition (Minshall et al, 1997; Elovic et al, 1998; Ando et al, 2010)
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