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Updated: Mar 1, 2026
Porphyromonas gingivalis as a Model Organism for Assessing Interaction of Anaerobic Bacteria with Host Cells
Published on: December 17, 2015
Respuesta mediada por ATF5 a la UPR mitocondrial inhibió RANKL en osteoblastos tratados con LPS de Porphyromonas
Tianrui Yang1, Weiman Sun2, Lang Lei2
1Shanghai Jiading District Central Hospital, Shanghai, China; Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.
Objective:
The purpose of this study was to investigate whether mitochondrial unfolded protein response (UPRmt) was induced in Porphyromonas gingivalis-lipopolysaccharide (P. gingivalis-LPS)-treated osteoblasts and to study the relationship among UPRmt, mitochondrial function and bone resorption in periodontitis.
Design:
Osteoblasts were treated with P.gingivalis-LPS. Nicotinamide riboside (NR) and doxycycline (DOX) were used to enhance UPRmt, while small interference RNA was transfected to knock down activating transcription factor 5 (ATF5). Protein and mRNA levels of genes involved in UPRmt and bone metabolism were measured. Intracellular reactive oxygen species (ROS), mitochondrial ROS and mitochondrial membrane potential were detected by flow cytometry and confocal imaging.
Results:
UPRmt and receptor activator of NF-κB ligand (RANKL) expression were induced in P. gingivalis-LPS-treated osteoblasts. Enhancement of UPRmt by NR or DOX decreased RANKL and RANKL/osteoprotegerin (OPG) ratio in osteoblasts. UPRmt inhibition by ATF5 knockdown aggravated mitochondrial dysfunction and promoted RANKL expression in P.gingivalis-LPS-treated osteoblasts.
Conclusions:
ATF5-mediated UPRmt regulates RANKL expression through mtROS and mitochondrial membrane potential. UPRmt could be a potential target involved in the regulation of bone resorption in periodontitis.
