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Fig. 5 | BMC Pulmonary Medicine

Fig. 5

From: DNA-PKcs modulates progenitor cell proliferation and fibroblast senescence in idiopathic pulmonary fibrosis

Fig. 5

Loss of PRKDC transcript and DNA damage response components in SSEA4+ and SSEA4− IPF fibroblasts. SSEA4+ cells were sorted from normal and IPF lung fibroblast cultures. RNA was extracted from the sorted cells SSEA4+ and non-sorted SSEA4− cells and subject to RNA sequencing analysis as previously described (GSE103488 [9]). a-b Shown are Ingenuity canonical pathway analysis of Rapid-IPF versus normal SSEA4+ cells (a) and Rapid-IPF versus normal SSEA4− cells (b). Ingenuity was set to consider transcripts with an FPKM value ≥0.2 and a fold change ≥1.5 & ≤ − 1.5 (a) and FPKM value ≥1 and a fold change ≥1.5 & ≤ − 1.5 (b). Percentage depicts the proportion of transcripts from the transcriptomic analysis that are annotated in the Ingenuity canonical pathway. The percentage of transcripts that are downregulated or upregulated in each canonical pathway are depicted in green or red, respectively. c-d Shown are the mean FPKM counts for PRKDC in normal, slow-IPF and rapid-IPF SSEA4+ progenitors (a) and SSEA4− fibroblasts (b). Data shown are mean ± s.e.m.; n = 2–5/group. *p ≤ 0.05 via Mann-Whitney two-tailed non-parametric test

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