ArticleBiochimica et biophysica acta2013
Mechanism of interleukin-1α transcriptional regulation of S100A9 in a human epidermal keratinocyte cell line.
Article in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Survival prediction in patients with head and neck squamous cell carcinoma and novel mechanistic insights of S100A8/A9.Discover oncology · 2024Article
- The Modulation of Septic Shock: A Proteomic Approach.International journal of molecular sciences · 2024Article
- Antimicrobial peptides: Defending the mucosal epithelial barrier.Frontiers in oral health · 2022Review
- The S100A10-AnxA2 complex is associated with the exocytosis of hepatitis B virus in intrauterine infection.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Overexpression of S100A9 in obesity impairs macrophage differentiation via TLR4-NFkB-signaling worsening inflammation and wound healing.Theranostics · 2022Article
- AHR Signaling Interacting with Nutritional Factors Regulating the Expression of Markers in Vascular Inflammation and Atherogenesis.International journal of molecular sciences · 2020Article
- S100-A9 protein in exosomes derived from follicular fluid promotes inflammation via activation of NF-κB pathway in polycystic ovary syndrome.Journal of cellular and molecular medicine · 2020Article
- Article
- Calprotectin and the Initiation and Progression of Head and Neck Cancer.Journal of dental research · 2018Review
- Regulatory mechanism and functional analysis of S100A9 in acute promyelocytic leukemia cells.Frontiers of medicine · 2017Article
- S100 Proteins As an Important Regulator of Macrophage Inflammation.Frontiers in immunology · 2017Review
- Autonomous immunity in mucosal epithelial cells: fortifying the barrier against infection.Microbes and infection · 2016Review
- SERPINB3/B4 contributes to early inflammation and barrier dysfunction in an experimental murine model of atopic dermatitis.The Journal of investigative dermatology · 2015Article
- Article
- Recent advances in host defense mechanisms/therapies against oral infectious diseases and consequences for systemic disease.Advances in dental research · 2014Review
- Transition metal ions at the crossroads of mucosal immunity and microbial pathogenesis.Frontiers in cellular and infection microbiology · 2014Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
S100A9 is a calcium-binding protein and subunit of antimicrobial calprotectin complex (S100A8/A9). Produced by neutrophils, monocytes/macrophages and keratinocytes, S100A9 expression increases in response to inflammation. For example, IL-1α produced by epithelial cells acts autonomously on the same cells to induce the expression of S100A8/A9 and cellular differentiation. Whereas it is well known that IL-1α and members of the IL-10 family of cytokines upregulate S100A8 and S100A9 in several cell lineages, the pathway and mechanism of IL-1α-dependent transcriptional control of S100A9 in epithelial cells are not established. Modeled using human epidermal keratinocytes (HaCaT cells), IL-1α stimulated the phosphorylation of p38 MAPK and induced S100A9 expression, which was blocked by IL-1 receptor antagonist, RNAi suppression of p38, or a p38 MAPK inhibitor. Transcription of S100A9 in HaCaT cells depended on nucleotides -94 to -53 in the upstream promoter region, based upon the use of deletion constructs and luciferase reporter activity. Within the responsive promoter region, IL-1α increased the binding activity of CCAAT/enhancer binding protein β (C/EBPβ). Mutated C/EBPβ binding sequences or C/EBPβ-specific siRNA inhibited the S100A9 transcriptional response. Hence, IL-1α is strongly suggested to increase S100A9 expression in a human epidermal keratinocyte cell line by signaling through the IL-1 receptor and p38 MAPK, increasing C/EBPβ-dependent transcriptional activity.
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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.