Awards
Best Poster Award at the 21st Conference of the Japanese Society of Pathology (Assistant Professor Takashima Takeshi, Department of Molecular Pathology)
Assistant Professor Takashima Tsuyoshi of the Department of Pathology and Molecular Pathology at our university won the Best Poster Award at the 21st Japanese Society of Pathology Conference held on July 25th and 26th, 2025.
Awarding Organization
Japanese Society of Pathology
Award-winning Abstract
The long non-coding RNA MIR205HG, which is upregulated in idiopathic pulmonary fibrosis, regulates IL33 expression
Research Overview and Background
Idiopathic pulmonary fibrosis is an intractable lung disease characterized by histological structural changes such as fibrosis(*1) in the distal lung. Effective therapeutic drugs are yet to be developed, and the development of a new treatment based on a novel pathological mechanism is anticipated. It has been previously reported that basal cells appear in the distal lung, and an increase in basal cells indicates a poor prognosis, but the mechanism by which basal cells contribute to the pathology has not been fully elucidated.
Research Methods and Results
In this study, we reanalyzed public single-cell RNA-sequencing data from normal lungs and patients with idiopathic pulmonary fibrosis to identify a long non-coding RNA, MIR205HG, highly expressed in basal cells. Prognostic analysis of idiopathic pulmonary fibrosis patient samples revealed that patients with high MIR205HG expression had a significantly poorer prognosis. Furthermore, we found that MIR205HG positively regulated IL33 expression by knockdown of MIR205HG in primary cultured basal cell-derived cells and organoids, or by overexpression of MIR205HG in alveolar epithelial organoids that do not express MIR205HG. The AluJb element of MIR205HG was crucial for regulating IL33 expression. Recently, it has been reported that IL33 promotes fibrosis by inducing type 2 innate lymphoid cells (ILC2s) in a mouse model of pulmonary fibrosis. We investigated the relationship between MIR205HG and ILC2 in idiopathic pulmonary fibrosis patient samples and found an increase in ILC2 in the MIR205HG-high expression group. These results suggest that MIR205HG, which is highly expressed in basal cells, may contribute to the pathogenesis of idiopathic pulmonary fibrosis by increasing IL33 expression.
(*1) Fibrosis: The proliferation of fibrous tissue, which replaces tissue with fibrous components and hardens it.