ArticleEBioMedicine2019
Dual function of miR-1248 links interferon induction and calcium signaling defects in Sjögren's syndrome.
Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- Molecular classification of primary Sjögren's syndrome based on salivary gland omics.Arthritis research & therapy · 2026Article
- Updating on the Dual Role of Salivary Gland Epithelial Cell (SGEC) in Sjögren's Disease.Journal of inflammation research · 2025Review
- Salivary gland transcriptomic analysis and immunophenotyping in the IL-14α transgenic mouse model of Sjögren's disease.Frontiers in dental medicine · 2025Article
- Deciphering miRNA signatures in axial spondyloarthritis: The link between miRNA-1-3p and pro-inflammatory cytokines.Heliyon · 2024Article
- Primary Sjögren's syndrome: new perspectives on salivary gland epithelial cells.European journal of medical research · 2024Review
- Inhibition of JAK-STAT pathway corrects salivary gland inflammation and interferon driven immune activation in Sjögren's disease.Annals of the rheumatic diseases · 2024Article
- Role of ncRNAs in the Pathogenesis of Sjögren's Syndrome.Biomedicines · 2024Review
- Identification of circRNA-associated ceRNA networks in peripheral blood mononuclear cells as potential biomarkers for chronic obstructive pulmonary disease.Bioscience reports · 2023Article
- Inhibition of CD4 + T cells by fanchinoline via miR506-3p/NFATc1 in Sjögren's syndrome.Inflammopharmacology · 2023Article
- MicroRNAs in the Regulation of RIG-I-like Receptor Signaling Pathway: Possible Strategy for Viral Infection and Cancer.Biomolecules · 2023Review
- Review
- Inflammasomes and their roles in arthritic disease pathogenesis.Frontiers in molecular biosciences · 2022Review
- MicroRNA-Mediated Epigenetic Regulation of Rheumatoid Arthritis Susceptibility and Pathogenesis.Frontiers in immunology · 2022Review
- Interaction Between Non-Coding RNAs and Interferons: With an Especial Focus on Type I Interferons.Frontiers in immunology · 2022Review
- Review
- Making Sense of Intracellular Nucleic Acid Sensing in Type I Interferon Activation in Sjögren's Syndrome.Journal of clinical medicine · 2021Review
- A survey of transcripts generated by spinal muscular atrophy genes.Biochimica et biophysica acta. Gene regulatory mechanisms · 2020Review
- Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSjögren's syndrome (SS) is one of the most common autoimmune disorders leading to exocrine gland dysfunction. Both immune-dependent processes - like Type I Interferon (IFN) signaling and immune-independent processes - such as calcium signaling in epithelial cells - contribute to disease pathophysiology. However, a mechanistic link between these processes has not been demonstrated.
methodsPrimary human salivary gland cells were used to evaluate the differential expression of miRNAs with smRNA-seq in primary epithelial cells culture and digital PCR was conducted in SS human salivary glands (SG) biopsies to verify the results. With siRNA screening and pull-down assays to establish the role of miRNA in IFN activation.
findingsActivation of IFN-β by miR-1248 is through the direct association with both RIG-I and AGO2. Further functional studies establish a unique dual functional role of miR-1248 in phSG cells: i) activation of the RIG-I pathway by acting as ligand of this sensor leading to IFN production and ii) regulation of the expression of mRNAs through the canonical microRNA function. Importantly, ITPR3, a key component of calcium signaling in epithelial cells, that has previously shown to be downregulated in SS SG, was directly targeted and downregulated by miR-1248, inducing the same functional calcium signaling changes as observed in SS SGs.
interpretationIdentification of the first endogenous mammalian microRNA that binds to RIG-I inducing IFN production but also demonstrate a novel pathophysiological underlying mechanism in which miR-1248 overexpression links two major pathways associated with SS, namely activation of IFN production with modulation of calcium signaling. Together, these findings suggest a unifying hypothesis for the immune-independent and -dependent processes contributing to the pathogenesis of SS. FUND: This research was supported by the Intramural Research Program of the National Institutes of Health (NIH), National Institute of Dental and Craniofacial Research (NIDCR).
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