Gene expression profiles of mitochondria-endoplasmic reticulum tethering in human gingival fibroblasts in response to periodontal pathogens

The current study aimed to elucidate the potential involvement of mitochondria-endoplasmic reticulum contact genes in pathogenesis periodontal disease by monitoring levels associated including Mitofusion 1 (MFN1) and MFN2, inositol 1,4,5-trisphosphate receptor (IP3R), chaperone glucose-regulated protein 75 (GRP75), sigma non-opioid intracellular (SIGMAR1) phosphate tensin homolog induced putative kinase (PINK1) human gingival fibroblasts response pathogens Fusobacterium nucleatum (F. nucleatum) Porphyromonas gingivalis (P. gingivalis) vitro. Primary were exposed live cultures P. (W83; ATCC BAA-308) F. (subsp. Polymorphum; 10953) alone or combination for 4 h at a 50 200 multiplicity infection. Escherichia coli lipopolysaccharide (10 μg/mL) exposure was used as positive control. Gene expression (MFN1, IP3R, GRP75, SIGMAR1 PINK1) well proinflammatory cytokine, Tumor necrosis factor-α (TNF-α), apoptosis gene, Immediate early 3 (IER3), evaluated reverse transcription polymerase chain reaction analysis. MFN1, IP3R PINK1 significantly upregulated with without nucleatum. Only caused significant upregulation SIGMAR1. TNF-α IER3 gene positively correlated contact-associated changes. may differentially dysregulate fibroblasts. These host-microbiome interactions mechanistically be important disease.