Abstract
This study was designed to explore the role of lncRNA LINC00616 in the regulation of periodontitis. Cellular functions were measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assays. The content of reactive oxygen species, Fe2+, glutathione, and malondialdehyde were measured to determine ferroptosis in Porphyromonas gingivalis lipopolysaccharide (LPS-PG) treated periodontal ligament stem cells (PDLSCs), as well as expression of glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11, and acyl-CoA synthetase long-chain family member 4 proteins mRNA and miRNA levels were measured by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). Western blot analysis was performed to assess protein expression. Targeting relationships were predicted using StarBase and TargetScan and verified by a dual luciferase reporter assay. The lncRNA LINC00616 was upregulated in periodontitis ligament tissues of patients with periodontitis and in PDLSCs treated with LPS-PG. Inhibition of LINC00616 promoted cell viability and suppressed ferroptosis of PDLSCs. miR-370 was verified to be a target of LINC00616, and suppressed miR-370 reversed the effects of LINC00616 knockdown on cell viability and ferroptosis in PDLSCs. Additionally, miR-370 targeting the transferrin receptor protein and upregulated transferrin receptor (TFRC) abolished the effects of overexpressed miR-370 on cell viability and ferroptosis of PDLSCs. LINC00616 acted as a competitive endogenous RNA (ceRNA) to promote ferroptosis of PDLSCs via the miR-370/TFRC axis. Therefore, LINC00616 knockdown may be a promising therapeutic strategy for periodontitis.