NCOA4‐mediated ferritinophagy promoted inflammatory responses in periodontitis

• DOI: 10.1111/jre.12852
• Publication Date: 2021-02-06T12:40:42Z
• Authors: Wei Guo; Yunhe Zhao; Houxuan Li; Lang Lei
• Keywords: Transferrin receptor

Iron homeostasis plays a crucial role in the combat against pathogen invasion. Ferrous iron can trigger generous production of reactive oxygen species (ROS) by Fenton reaction. Nuclear receptor coactivator 4 (NCOA4), selective cargo to deliver ferritin lysosome, may release ferritin-bound into cytosol. The aim present study was explore whether NCOA4-mediated ferritinophagy participated pathogenesis periodontitis, and its promoting periodontal inflammation.Inflamed healthy tissues were harvested for immunobiological staining ferritinophagy-related genes tissues, while real-time quantitative PCR (qPCR) utilized detect mRNA transcription. Periodontal ligament fibroblasts (PDLFs) isolated infected with Porphyromonas gingivalis. transcription protein expression involved metabolism, including NCOA4, transferrin 1 (TFR1), ferroportin (SLC40A1) detected qPCR western blot. Levels labile pool ROS flow cytometry confocal endoscopy. Small interference RNA knock down NCOA4.Elevated heavy chain, light chain observed diseased tissues. P. gingivalis infection promoted TFR1, microtubule-associated 1-light 3 B (LC3B), enhanced levels intracellular production. NCOA4 knockdown reduced generation PDLFs response mitigated pro-inflammatory monocyte chemoattractant protein-1 interleukin 6. triggered activation c-Jun N-terminal kinase (JNK) p38 mitogen-activated signaling pathway. In addition, inhibitors JNK, SP600125, p38, SB203580 blocked transcription.NCOA4-ferritinophagy progress periodontitis progression. gingvalis-triggered aggravated inflammatory responses PDLFS. These findings suggest an important periodontitis.