Abstract

<b>Background:</b> The injury to airway epithelium causes loss of its structural integrity and function as a barrier. Severe or continuous injury, observed in chronic inflammation of the airways, disturbs the repair process, increasing permeability for environmental factors. The process of wound repair is complex and requires the phased expression of networks of genes. The main aim of our study was to observe whether there are alterations in human transcriptome during the repair of bronchial epithelial cells. <b>Methods:</b> We analyzed the changes in transcriptome during the wound repair in a cell culture model of human bronchial epithelium. Gene expression was identified at several time points: before the injury and 4, 8, 16, 24 hours after injury with SurePrint G3 Human Gene Expression whole transcriptome microarrays. Data were analyzed using Gene Spring 14.9 software. <b>Results:</b> The expression levels of 11034 genes were significantly altered during the wound repair process (fold change&gt;2.0, p&lt;0.05). Bioinformatic analysis has revealed 69 significant GO terms, related to cell communication, adhesion, proliferation and differentiation. Pathway Analysis has revealed 57 significantly enriched pathways, for example: olfactory receptor activity, inflammatory response, lung fibrosis, MAPK signalling pathway, signaling of interleukin-10, interleukin-4 and interleukin-13, and interestingly, innate immunity related to SARS-CoV2. <b>Conclusion:</b> Human transcriptome is altered during wound repair in airway epithelium in vitro, revealing the genetic mechanisms of this process, suggesting pathways potentially relevant in abnormal wound repair. This study was supported by the Polish National Science Centre grant no. 2017/25/N/NZ3/00332.

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