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Involvement of lncRNA MIR205HG in idiopathic pulmonary fibrosis and regulation of IL33 via Alu elements (part 2)

GSE275709 Homo sapiens Expression profiling by high throughput sequencing 4 samples Submitted 2025/03/10 Platform GPL24676
Summary
Idiopathic pulmonary fibrosis (IPF) causes remodelling of distal lung, leading to respiratory failure. Pulmonary remodelling is characterised histologically not only by fibrosis but by also appearance of basal cells, yet the involvement of basal cells to IPF pathogenesis remains unclear. Here, we focus on the long non-coding RNA MIR205HG highly expressed in basal cells by single-cell RNA sequencing, to elucidate their role in IPF. Through RNA sequencing of genetic manipulations using primary cells and IPF-derived airway organoids, we uncovered MIR205HG to regulate IL33 expression. Mechanistically, the AluJb element of MIR205HG plays a key role in IL33 expression. In addition, we successfully identified a small molecule that targets this AluJb element and decreases IL33 expression. IL33 is known to induce ILC2, and MIR205HG expression positively correlated with the number of ILC2 in IPF patients. Collectively, these findings provide insights into the contributing mechanisms of basal cells to IPF and potential therapeutic targets.
Published in
Involvement of lncRNA MIR205HG in idiopathic pulmonary fibrosis and IL-33 regulation via Alu elements
Takashima T, Zeng C, Murakami E et al. · JCI insight 2025 · PMID 40059822 · doi:10.1172/jci.insight.187172
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Also filed as BioProject PRJNA1152602 and SRA study SRP528764. Searching any of these in the dataset finder brings you back here.

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