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    Evaluation of the role of mitofusin-1 and mitofusin-2 in periodontal disease
    (Wiley, 2024) Kirmiziguel, Omer Alperen; Sabanci, Arife; Disli, Faruk; Yildiz, Sedat; Milward, Michael R.; Aral, Kubra
    BackgroundMitochondria and endoplasmic reticulum are key cellular organelles and create contact sites (mitochondria-endoplasmic reticulum contact [MERC]), which plays a major role in calcium metabolism, apoptotic processes, and inflammation. Previously, proteins that have been associated with these MERC contact sites mitofusin-1 (MFN1) and mitofusin-2 (MFN2) have been found to be downregulated in periodontal disease in vitro. Therefore, the aim of the current study was to evaluate MFN1 and MFN2 in gingival crevicular fluid (GCF) of patients with periodontal disease compared with healthy controls clinically. MethodsA total of 48 participants were divided into three groups including periodontally healthy (n = 16), patients with gingivitis (n = 16), and patients with stage 3 grade B periodontitis (n = 16). GCF levels of MFN1, MFN2, calcium (Ca), caspase-1, and tumor necrosis factor-alpha (TNF-& alpha;) were determined via enzyme-linked immunosorbent assay (ELISA). Results were calculated as total amount and concentration. ResultsMFN1 levels (total amount) were significantly higher in patients with periodontitis and gingivitis when compared with healthy controls (p < 0.05). However, concentration levels of MFN1, MFN2, Ca, caspase-1, TNF-& alpha; significantly decreased in periodontal disease groups compared with healthy controls (p < 0.05). A positive correlation was detected among all evaluated markers (p < 0.05). ConclusionThe MERC protein MFN1 may have a role in the pathogenesis of periodontal disease due to its increase in GCF of patients with periodontitis and gingivitis.
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    Gene expression profiles of mitochondria-endoplasmic reticulum tethering in human gingival fibroblasts in response to periodontal pathogens
    (Pergamon-Elsevier Science Ltd, 2021) Aral, Kubra; Milward, Michael R.; Cooper, Paul R.
    Objective: The current study aimed to elucidate the potential involvement of mitochondria-endoplasmic reticulum contact genes in the pathogenesis of periodontal disease by monitoring levels of contact associated genes including Mitofusion 1 (MFN1) and MFN2, inositol 1,4,5-trisphosphate receptor (IP3R), chaperone glucoseregulated protein 75 (GRP75), sigma non-opioid intracellular receptor 1 (SIGMAR1) and phosphate and tensin homolog induced putative kinase 1 (PINK1) in human gingival fibroblasts in response to periodontal pathogens Fusobacterium nucleatum (F. nucleatum) and Porphyromonas gingivalis (P. gingivalis) in vitro. Design: Primary human gingival fibroblasts were exposed to live cultures of P. gingivalis (W83; ATCC BAA-308) and F. nucleatum (subsp. Polymorphum; ATCC 10953) alone or in combination for 4 h at a 50 or 200 multiplicity of infection. Escherichia coli lipopolysaccharide (10 mu g/mL) exposure was used as a positive control. Gene expression levels of contact genes (MFN1, MFN2, IP3R, GRP75, SIGMAR1 and PINK1) as well as a proinflammatory cytokine, Tumor necrosis factor-alpha (TNF-alpha), and the apoptosis associated gene, Immediate early response 3 (IER3), were evaluated by reverse transcription polymerase chain reaction analysis. Results: MFN1, GRP75, IP3R and PINK1 were significantly upregulated by P. gingivalis with or without F. nucleatum. Only P. gingivalis with F. nucleatum caused a significant upregulation of SIGMAR1. TNF-alpha and IER3 gene expression positively correlated with the contact-associated gene expression changes. Conclusion: F. nucleatum and P. gingivalis alone or in combination may differentially dysregulate the gene expression levels of contact-associated genes in human gingival fibroblasts. These host-microbiome interactions may mechanistically be important in the pathogenesis of periodontal disease.