ArticleBMJ open respiratory research2024
Pim1 inactivating induces RUNX3 upregulation that improves/alleviates airway inflammation and mucus hypersecretion in vitro and in vivo.
Article in BMJ open respiratory research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- PIM1 Inhibition Alleviates Aspergillus fumigatus Keratitis by Regulating DDX41-Mediated STING Signaling Pathway.Investigative ophthalmology & visual science · 2026Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeOur research aimed to evaluate whether proto-oncogene serine/threonine-protein kinase Pim-1 (Pim1) inactivation could attenuate asthma by promoting runt-related transcription factor 3 (Runx3) expression and explore the underlying molecular mechanism.
methodPhorbol 12-myristate 13-acetate (PMA, 50 nM) was used to induce inflammation in BEAS-2B human airway epithelial cells. ELISA and immunofluorescence double staining confirmed inflammation modelling and differential expression of Pim1 and Runx3. Pim1 inhibitor (SGI-1776) and Runx3 siRNA (siRunx3) were used in this study. Apoptosis, inflammation, MUC5AC protein expression, Pim1 kinase and Runx3 protein expression, and PI3K/AKT/nuclear factor-κB (NF-κB) pathway-associated protein expression were also assessed by flow cytometry, immunofluorescence and western blot. The effects of Pim1 inactivation on airway inflammation, pathological injury and mucus secretion in wild-type and Runx3 knockout mice were observed by in vivo experiments.
resultsThe results of the in vitro experiments showed that PMA stimulation causes BEAS-2B cell apoptosis and promotes the MUC5AC expression. In addition, PMA stimulation activated the PI3K/AKT/NF-κB pathway. SGI-1776 treatment partially reversed these effects, whereas siRunx3 attenuated the effects of SGI-1776 on PMA-stimulated BEAS-2B cells. In vivo experiments showed that in Runx3-KO asthmatic mice, inhibition of Pim1 kinase had less effect on airway inflammation, pathological injury and mucus secretion. Meanwhile, Pim1 kinase expression was higher in Runx3-KO asthmatic mice than in wild-type asthmatic mice. Furthermore, inhibition of Pim1 kinase inhibited activation of the PI3K/AKT/NF-κB pathway, whereas these effects were attenuated in Runx3-KO mice.
conclusionOur results suggest that Pim1 inactivation can ameliorate airway inflammation and mucus hypersecretion through upregulation of Runx3 and the effect could be mediated through modulation of the PI3K/AKT/NF-κB pathway.
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