Fig. 1: HOTAIRM1 is increased in lung tissues of IPF mice and initiates IPF. | Laboratory Investigation

Fig. 1: HOTAIRM1 is increased in lung tissues of IPF mice and initiates IPF.

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

Fig. 1

A Correlation between the expression of HOTAIRM1 and HSF1 in lung tissues in GTEx in the GEPIA database. B HOTAIRM1 expression in normal (n = 35) and IPF samples (n = 49) in the GSE124685 dataset. C RT–qPCR detection of HOTAIRM1 expression in lung tissues of normal (n = 6) and IPF mice (n = 6). D RT–qPCR detection of HOTAIRM1 expression in lung tissues of IPF mice treated with oe-HOTAIRM1 or sh-HOTAIRM1. E Lung compliance and resistance in lung tissues of normal mice and IPF mice treated with oe-HOTAIRM1 or sh-HOTAIRM1. F Western blot analysis of α-SMA, collagen I, and fibronectin proteins in lung tissues of IPF mice treated with oe-HOTAIRM1 or sh-HOTAIRM1. G Level of hydroxyproline in the lung tissue of IPF mice treated with oe-HOTAIRM1 or sh-HOTAIRM1. n = 6 for mice upon each treatment. The data are shown as the mean ± standard deviation. Data between two groups were analyzed by unpaired t test, while those among multiple groups were assessed by one-way ANOVA with Tukey’s post-hoc tests. *p < 0.05, compared with normal mice. #p < 0.05, compared with oe-NC-treated mice. &p < 0.05, compared with sh-NC-treated mice.

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