Fig. 4: HOTAIRM1 binds to miR-30d-3p and consequently increases the expression of the miR-30d-3p target HSF1. | Laboratory Investigation

Fig. 4: HOTAIRM1 binds to miR-30d-3p and consequently increases the expression of the miR-30d-3p target HSF1.

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

Fig. 4

A Venn diagram of the predicted miRNAs binding to HOTAIRM1 and HSF1 by the LncBase and miRWalk databases. B Putative binding sites between miR-30d-3p and HOTAIRM1 and HSF1. C RT–qPCR detection of miR-30d-3p expression in the lung tissues of normal (n = 6) and IPF mice (n = 6). D Binding between HOTAIRM1 and miR-30d-3p confirmed by a dual-luciferase reporter assay in HEK-293T cells. E Subcellular colocalization of HOTAIRM1 and miR-30d-3p analyzed by FISH assay. F RT–qPCR detection of miR-30d-3p expression in the presence of oe-HOTAIRM1 or sh-HOTAIRM1. G Binding between HSF1 and miR-30d-3p confirmed by a dual-luciferase reporter assay in HEK-293T cells. H RT–qPCR detection of HSF1 expression in the presence of miR-30d-3p mimic or miR-30d-3p inhibitor. The data are shown as the mean ± standard deviation of three technical replicates. 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 or treatment with mimic NC or oe-NC. #p < 0.05, compared with treatment with sh-NC or inhibitor NC.

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