Fig. 5: HOTAIRM1 enhances the proliferation and transdifferentiation of LFs through the miR-30d-3p/YY1/HSF1 axis. | Laboratory Investigation

Fig. 5: HOTAIRM1 enhances the proliferation and transdifferentiation of LFs through the miR-30d-3p/YY1/HSF1 axis.

From: Exosomes derived from hypoxia-induced alveolar epithelial cells stimulate interstitial pulmonary fibrosis through a HOTAIRM1-dependent mechanism

Fig. 5

A RT–qPCR detection of HOTAIRM1, YY1, HSF1, and miR-30d-3p expression in LFs treated with oe-HOTAIRM1 + sh-NC or oe-HOTAIRM1 + sh-HSF1. B CCK-8 detection of the proliferation of LFs treated with oe-HOTAIRM1 + sh-NC or oe-HOTAIRM1 + sh-HSF1. C Western blot analysis of α-SMA, collagen I, fibronectin, Ki67, and PCNA proteins in LFs treated with oe-HOTAIRM1 + sh-NC or oe-HOTAIRM1 + sh-HSF1. D Immunofluorescence analysis of α-SMA, collagen I, fibronectin, Ki67, and PCNA proteins in LFs treated with oe-HOTAIRM1 + sh-NC or oe-HOTAIRM1 + sh-HSF1. The data are shown as the mean ± standard deviation of three technical replicates. Data among multiple groups were assessed by one-way ANOVA with Tukey’s post-hoc tests. Repeated measures ANOVA with Tukey’s post-hoc test was applied for the comparison of data at different time points. *p < 0.05, compared with treatment with oe-NC + sh-NC. #p < 0.05, compared with treatment with oe-HOTAIRM1 + sh-NC.

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