ArticleRheumatology international2013
TLR3-mediated apoptosis and activation of phosphorylated Akt in the salivary gland epithelial cells of primary Sjögren's syndrome patients.
Article in Rheumatology international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Akt Signaling Pathway Is Activated in the Minor Salivary Glands of Patients with Primary Sjögren's Syndrome.International journal of molecular sciences · 2021Trial
- Mechanistic exploration of bisphenol A in primary Sjögren's syndrome using network toxicology, molecular docking, molecular dynamics simulations and experimental validation.BMC pharmacology & toxicology · 2025Article
- Updating on the Dual Role of Salivary Gland Epithelial Cell (SGEC) in Sjögren's Disease.Journal of inflammation research · 2025Review
- Review
- A comprehensive review of Sjögren's syndrome: Classification criteria, risk factors, and signaling pathways.Heliyon · 2024Review
- Primary Sjögren's syndrome: new perspectives on salivary gland epithelial cells.European journal of medical research · 2024Review
- Current Views on Pathophysiology and Potential Therapeutic Targets in Sjögren's Syndrome: A Review from the Perspective of Viral Infections, Toll-like Receptors, and Long-Noncoding RNAs.Journal of clinical medicine · 2023Review
- The Role of the Akt Signaling Pathway in Sjögren's Syndrome.Mediterranean journal of rheumatology · 2023Article
- Review
- Immune complexome analysis reveals the presence of immune complexes and identifies disease-specific immune complex antigens in saliva samples from patients with Sjögren's syndrome.Clinical and experimental immunology · 2021Article
- Role of the Innate Immunity Signaling Pathway in the Pathogenesis of Sjögren's Syndrome.International journal of molecular sciences · 2021Review
- Contributions of Major Cell Populations to Sjögren's Syndrome.Journal of clinical medicine · 2020Review
- Activation of Myd88-Dependent TLRs Mediates Local and Systemic Inflammation in a Mouse Model of Primary Sjögren's Syndrome.Frontiers in immunology · 2019Article
- Modulation of Apoptosis by Cytotoxic Mediators and Cell-Survival Molecules in Sjögren's Syndrome.International journal of molecular sciences · 2018Review
- Current and Emerging Evidence for Toll-Like Receptor Activation in Sjögren's Syndrome.Journal of immunology research · 2018Review
- Myd88 is required for disease development in a primary Sjögren's syndrome mouse model.Journal of leukocyte biology · 2017Article
- Leptin/OB-R pathway promotes IL-4 secretion from B lymphocytes and induces salivary gland epithelial cell apoptosis in Sjögren's syndrome.Oncotarget · 2017Article
- Innate immunity in Sjögren's syndrome.Clinical immunology (Orlando, Fla.) · 2017Review
- Reviewing primary Sjögren's syndrome: beyond the dryness - From pathophysiology to diagnosis and treatment.International journal of medical sciences · 2017Review
- Innate Immune Signaling Induces IL-7 Production, Early Inflammatory Responses, and Sjögren's-Like Dacryoadenitis in C57BL/6 Mice.Investigative ophthalmology & visual science · 2015Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed at ascertain whether innate immunity is involved in the apoptosis of primary cultured salivary gland epithelial cells (SGECs) in primary Sjögren's syndrome (pSS). Induction of apoptosis of SGECs was performed using a TLR3 ligand, poly (I:C). Activation of phosphorylated-Akt (pAkt) and cleaved-caspase 3 was determined by Western blotting or immunofluorescence. Expression of TLR2 and TLR3 with pAkt was observed in cultured SGECs after 24-h stimulation with each ligand. Compared with stimulation with the peptidoglycan or lipopolysaccharide, that with poly (I:C) induced significant nuclear fragmentation, as determined by Hoechst staining (p = 0.0098). Apoptosis was confirmed by terminal deoxynucleotidyltransferase-mediated dUTP nick end-labeling (TUNEL) staining of SGECs from pSS patients and a normal subject. A significant increase in TUNEL-positive cells was observed by the addition of a PI3K inhibitor, LY294002. Poly (I:C) phosphorylated stress-activated protein kinase/Jun-terminal kinase and p44/42 MAP kinase as well as Akt. Furthermore, poly (I:C)-induced caspase 3 cleavage in SGECs was also inhibited by LY294002. Similar results were obtained using SGECs obtained from a normal subject. The results demonstrated for the first time that TLR3 induces the apoptotic cell death of SGECs via the PI3K-Akt signaling pathway.
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Registered trials
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