Artikel ; Online: Epithelial IL5RA promotes epithelial-mesenchymal transition in pulmonary fibrosis via Jak2/STAT3 cascade.
Pulmonary pharmacology & therapeutics
2024 Band 84, Seite(n) 102286
Abstract: Pulmonary fibrosis is a progressive and debilitating lung disease characterized by the excessive accumulation of extracellular matrix (ECM) components within the lung parenchyma. However, the underlying mechanism remains largely elusive, and the ... ...
Abstract | Pulmonary fibrosis is a progressive and debilitating lung disease characterized by the excessive accumulation of extracellular matrix (ECM) components within the lung parenchyma. However, the underlying mechanism remains largely elusive, and the treatment options available for pulmonary fibrosis are limited. Interleukin 5 receptor, alpha (IL5RA) is a well-established regulator of eosinophil activation, involved in eosinophil-mediated anti-parasitic activities and allergic reactions. Recent studies have indicated additional roles of IL5RA in lung epithelium and fibroblasts. Nevertheless, its involvement in pulmonary fibrosis remains unclear. In present study, we employed single-cell analyses alongside molecular and cellular assays to unveil the expression of IL5RA in lung epithelial cells. Moreover, using both in vitro and in vivo models, we demonstrated a notable upregulation of epithelial IL5RA during the progression of pulmonary fibrosis. This upregulated IL5RA expression subsequently promotes epithelial-mesenchymal transition (EMT), leading to the generation of mesenchymal phenotype with augmented capability for ECM production. Importantly, our findings uncovered that the pro-fibrotic function of IL5RA is mediated by Jak2/STAT3 signaling cascades. Inhibiting IL5RA has the potential to deactivate Jak2/STAT3 and suppress the downstream EMT process and ECM production, thereby offering a promising therapeutic strategy for pulmonary fibrosis. |
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Mesh-Begriff(e) | Humans ; Epithelial-Mesenchymal Transition/physiology ; Fibrosis ; Interleukin-5 Receptor alpha Subunit/metabolism ; Lung/metabolism ; Pulmonary Fibrosis/metabolism ; Receptors, Interleukin-5/metabolism ; STAT3 Transcription Factor/metabolism |
Chemische Substanzen | IL5RA protein, human ; Interleukin-5 Receptor alpha Subunit ; Receptors, Interleukin-5 ; STAT3 protein, human ; STAT3 Transcription Factor ; JAK2 protein, human (EC 2.7.10.2) |
Sprache | Englisch |
Erscheinungsdatum | 2024-01-06 |
Erscheinungsland | England |
Dokumenttyp | Journal Article |
ZDB-ID | 1399707-5 |
ISSN | 1522-9629 ; 1094-5539 |
ISSN (online) | 1522-9629 |
ISSN | 1094-5539 |
DOI | 10.1016/j.pupt.2024.102286 |
Datenquelle | MEDical Literature Analysis and Retrieval System OnLINE |
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