Sjögren's disease & overlap diseases
m6A RNA methylation controls salivary gland epithelial cell function and has a protective role in Sjögren's disease
Authors' conclusion
Impairment of m6A modifications in SGEC in response to inflammatory triggers favour the formation of dsRNA, potentially amplifying the interferon loop and contributing to SjD pathogenesis.
Study context
- Population
- Salivary gland epithelial cells (SGECs) from Sjögren's disease (SjD) patients and controls
- Comparison
- SGEC from SjD patients vs controls
Methodological detailsRNA-seq, quantitative PCR, immunohistochemistry, METTL3 knockdown or pharmacological inhibition, transwell and coculture systems, immunofluorescence, unsupervised clustering
- RNA-seq
- Quantitative PCR
- Immunohistochemistry
- METTL3 knockdown or pharmacological inhibition
- Transwell and coculture systems
- Immunofluorescence
- Unsupervised clustering
Main finding
As reported in the abstract
- METTL3 and METTL14 elevated in SGEC from SjD patients vs controls
- Inhibiting METTL3 increased proinflammatory gene expression, enhancing SGEC's ability to attract immune cells and activate B cells
- Inhibiting the eraser FTO had the opposite effect
- METTL3-mediated m6A modifications prevented double-stranded RNA (dsRNA) formation and IFN signalling activation
- SGEC from SjD showed insufficient METTL3 upregulation vs controls in response to inflammatory triggers
- SjD patients with elevated disease activity and higher interferon signature exhibit reduced METTL3 expression
Original publication
m6A RNA methylation controls salivary gland epithelial cell function and has a protective role in Sjögren's disease. Ann Rheum Dis. Published 25 September 2024. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →