ArticleInternational journal of molecular sciences2016
C/EBP β Mediates Endoplasmic Reticulum Stress Regulated Inflammatory Response and Extracellular Matrix Degradation in LPS-Stimulated Human Periodontal Ligament Cells.
Article in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 52 citations in OpenAlex.
- Identification of Endoplasmic Reticulum Stress-Related Biomarkers of Periodontitis Based on Machine Learning: A Bioinformatics Analysis.Disease markers · 2022Trial
- A genome-wide Mendelian randomization study focusing on endoplasmic reticulum stress reveals novel genetic markers for renal cell carcinoma.Oncology letters · 2026Article
- Transcriptomic response to compressive force simulating orthodontic tooth movement in cultured porcine epithelial cell rests of Malassez.Odontology · 2026Article
- Pharmacological investigation of bergapten isolated from Glehnia littoralis against periodontitis.Scientific reports · 2026Article
- Baicalin Alleviates LPS-Induced Apoptosis of Periodontal Ligament Cells Via Inhibiting Endoplasmic Reticulum Stress.International dental journal · 2026Article
- The Role of Endoplasmic Reticulum Stress in the Development of Periodontitis-From Experimental Cell and Animal Models to Humans.International journal of molecular sciences · 2025Review
- Single-Cell Transcriptomics Identified Fibrosis-Activated Valve Interstitial Cells Involved in Functional Tricuspid Regurgitation.JACC. Asia · 2025Article
- ERS-PERK Pathway is Involved in the Repair of the Pulpo-Dentinal Complex Under an Inflammatory Microenvironment.Stem cells international · 2025Article
- Role of periodontal ligament fibroblasts in periodontitis: pathological mechanisms and therapeutic potential.Journal of translational medicine · 2024Review
- Possible Involvement of X-Box Binding Protein-1 in the Onset of Pulpitis.European endodontic journal · 2024Article
- CD47 and thrombospondin-1 contribute to immune evasion byProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Discovering common pathogenetic processes between periodontitis and Alzheimer's disease by bioinformatics and system biology approach.BMC oral health · 2024Article
- Experimental periodontitis induced hypoadiponectinemia by IRE1α-mediated endoplasmic reticulum stress in adipocytes.BMC oral health · 2023Article
- Activation of BZW1 by CEBPB in macrophages promotes eIF2α phosphorylation-mediated metabolic reprogramming and endoplasmic reticulum stress in MRL/lpr lupus-prone mice.Cellular & molecular biology letters · 2023Article
- Identification of microRNA-mRNA-TF regulatory networks in periodontitis by bioinformatics analysis.BMC oral health · 2022Article
- The oral microbiome in young women at different stages of periodontitis:Frontiers in cellular and infection microbiology · 2022Article
- Loss of Dec1 prevents autophagy in inflamed periodontal ligament fibroblast.Molecular biology reports · 2021Article
- High Fat Diet Dysbiotic Mechanism of Decreased Gingival Blood Flow.Frontiers in physiology · 2021Article
- Autophagy, One of the Main Steps in Periodontitis Pathogenesis and Evolution.Molecules (Basel, Switzerland) · 2020Review
- Short-Chain Fatty Acids (Except Hexanoic Acid) Lower NF-kB Transactivation, Which Rescues Inflammation-Induced Decreased Apolipoprotein A-I Transcription in HepG2 Cells.International journal of molecular sciences · 2020Article
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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
Periodontitis is an oral inflammatory disease that not only affects the integrity of local tooth-supporting tissues but also impacts systemic health. A compositional shift in oral microbiota has been considered as the main cause of periodontitis; however, the potential mechanism has not been fully defined. Herein, we investigated the role of CCAAT/enhancer-binding protein β (C/EBP β), a member of the C/EBP family of transcription factors, in human periodontal ligament cells (hPDLCs) exposed to Porphyromonas gingivalis (P. gingivalis) lipopolysaccharide (LPS). RT-PCR and Western blotting analysis showed that the expression of C/EBP β was significantly increased in hPDLCs stimulated with LPS stimuli. Overexpression of C/EBP β by the recombinant adenoviral vector pAd/C/EBP β markedly increased the expression of the pro-inflammatory cytokines IL-6 and IL-8, and matrix metalloproteinases (MMP)-8 and -9 in hPDLCs in response to LPS. Furthermore, the activation of endoplasmic reticulum (ER) stress was confirmed in LPS-stimulated hPDLCs by measuring the expression of the ER stress marker molecules protein kinase-like ER kinase (PERK), eIF2α, GRP78/Bip, and C/EBP homologous protein (CHOP). The ER stress inhibitor salubrinal repressed, but inducer tunicamycin enhanced, the production of IL-6, IL-8, MMP-8, and MMP-9 in hPDLCs. Additionally, ER stress inducer tunicamycin significantly increased the expression level of C/EBP β in hPDLCs. Blocking of C/EBP β by siRNA resulted in a significant decrease in the secretion of IL-6 and IL-8 and expression of MMP-8 and MMP-9 induced by tunicamycin treatment in hPDLCs. Taken together, ER stress appears to play a regulatory role in the inflammatory response and extracellular matrix (ECM) degradation in hPDLCs in response to LPS stimuli by activating C/EBP β expression. This enhances our understanding of human periodontitis pathology.
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