ArticleJournal of cellular and molecular medicine2012
TNF-α inhibits aquaporin 5 expression in human salivary gland acinar cells via suppression of histone H4 acetylation.
Article in Journal of cellular and molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 61 citations in OpenAlex.
- Dexmedetomidine Dose-Dependent Modulation of Lung Function and AQP1 Expression During One-Lung Ventilation in Adults Undergoing Thoracoscopic Surgery.Medical science monitor : international medical journal of experimental and clinical research · 2025Trial
- Granzyme A-producing type 1 innate lymphoid cells promote salivary secretion in the aged submandibular gland.Inflammation and regeneration · 2026Article
- Psoriasis increases the risk of Sjögren's syndrome: evidence from a propensity score-matched cohort study and transcriptomic analysis.BMC medicine · 2025Article
- Nicotinamide mononucleotide suppresses cellular senescence and increases aquaporin 5 expression in the submandibular gland of aged male mice to ameliorate aging-related dry mouth.Biogerontology · 2024Article
- TNF inhibits AQP2 expression via a miR137-dependent pathway.American journal of physiology. Renal physiology · 2024Article
- Chemokines and lymphocyte homing in Sjögren's syndrome.Frontiers in immunology · 2024Review
- The involvement of aquaporin 5 in the inflammatory response of primary Sjogren's syndrome dry eye: potential therapeutic targets exploration.Frontiers in medicine · 2024Review
- Review
- Aquaporin-5 Dynamic Regulation.International journal of molecular sciences · 2023Review
- Aquaporins in Glandular Secretion.Advances in experimental medicine and biology · 2023Article
- Abnormal Histones Acetylation in Patients with Primary Sjögren's Syndrome.Clinical rheumatology · 2022Article
- Article
- Ruscogenin Ameliorated Sjögren's Syndrome by Inhibiting NLRP3 Inflammasome Activation.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Targeted Therapy for Primary Sjögren's Syndrome: Where are We Now?BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2021Review
- The Transcriptomic Profile of Monocytes from Patients With Sjögren's Syndrome Is Associated With Inflammatory Parameters and Is Mimicked by Circulating Mediators.Frontiers in immunology · 2021Article
- Review
- Inhibition of Alk signaling promotes the induction of human salivary-gland-derived organoids.Disease models & mechanisms · 2020Article
- Current State of Knowledge on Primary Sjögren's Syndrome, an Autoimmune Exocrinopathy.Journal of clinical medicine · 2020Review
- Insight into Salivary Gland Aquaporins.Cells · 2020Review
- Targeted TNF-α Overexpression Drives Salivary Gland Inflammation.Journal of dental research · 2019Article
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
Sjögren's syndrome is a systemic autoimmune disease characterized by reductions in salivary and lacrimal secretions. The mechanisms underlying these reductions remain unclear. We have previously shown that TNF-α plays an important role in the destruction of acinar structures. Here we examined TNF-α's function in the expression of aquaporin (AQP) 5 in human salivary gland acinar cells. Immortalized human salivary gland acinar (NS-SV-AC) cells were treated with TNF-α, and then the expression levels of AQP5 mRNA and protein were analysed. In addition, the mechanisms underlying the reduction of AQP5 expression by TNF-α treatment were investigated. TNF-α-treatment of NS-SV-AC cells significantly suppressed the expression levels of AQP5 mRNA and protein, and reduced the net fluid secretion rate. We examined the expression and activation levels of DNA methyltransferases (Dnmts) in NS-SV-AC cells treated with TNF-α. However, no significant changes were observed in the expression or activation levels of Dnmt1, Dnmt3a or Dnmt3b. Although we also investigated the role of NF-κB activity in the TNF-α-induced suppression of AQP5 expression in NS-SV-AC cells, we detected similar TNF-α suppression of AQP5 expression in non-transfected cells and in a super-repressor form of IκBα cDNA-transfected cell clones. However, interestingly, chromatin immunoprecipitation analysis demonstrated a remarkable decrease in levels of acetylated histone H4 associated with the AQP5 gene promoter after treatment with TNF-α in NS-SV-AC cells. Therefore, our results may indicate that TNF-α inhibition of AQP5 expression in human salivary gland acinar cells is due to the epigenetic mechanism by suppression of acetylation of histone H4.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.