Oral diseases · 2025
SMURF1 Regulates Periodontal Stem Cell Injury and Osteogenic Differentiation by Regulating TRAF4.
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Wei Ziming, Xiao Hui, Zhou Lishu, Wang Yarong
Аннотация
OBJECTIVE: This study aimed to investigate the specific role and mechanistic actions of tumor necrosis factor receptor-associated factor 4 (TRAF4) in periodontitis.
METHODS: Human periodontal ligament stem cells (PDLSCs) were exposed to lipopolysaccharide (LPS). Then, real-time quantitative polymerase chain reaction (RT-qPCR) and western blotting (WB) were carried out to determine the mRNA and protein expression levels of Smad ubiquitination regulator 1 (SMURF1). The relationship between TRAF4 and SMURF1, as predicted by the STRING and GeneMANIA databases, was verified by co-immunoprecipitation (Co-IP). Finally, both TRAF4 and SMURF1 were inhibited in PDLSCs by cell transfection, and the regulatory mechanisms involved were investigated by cell counting kit-8 assays, enzyme linked immunosorbent assay, WB, alkaline phosphatase, and alizarin red staining.
RESULTS: The gene and protein expression levels of SMURF1 in PDLSCs increased following LPS induction (p < 0.001); cell viability was decreased (p < 0.001), TRAF4 expression was decreased (p < 0.001), and cell-mineralized nodules were inhibited. Inhibition of SMURF1 expression increased PDLSCs activity and TRAF4 expression levels (p < 0.001), increased the number of cell-mineralized nodules, and enhanced cellular osteogenic capacity (p < 0.001).
CONCLUSIONS: SMURF1 regulates LPS-stimulated injury and improves the capacity for osteogenic differentiation in PDLSCs by downregulating the expression of TRAF4.
METHODS: Human periodontal ligament stem cells (PDLSCs) were exposed to lipopolysaccharide (LPS). Then, real-time quantitative polymerase chain reaction (RT-qPCR) and western blotting (WB) were carried out to determine the mRNA and protein expression levels of Smad ubiquitination regulator 1 (SMURF1). The relationship between TRAF4 and SMURF1, as predicted by the STRING and GeneMANIA databases, was verified by co-immunoprecipitation (Co-IP). Finally, both TRAF4 and SMURF1 were inhibited in PDLSCs by cell transfection, and the regulatory mechanisms involved were investigated by cell counting kit-8 assays, enzyme linked immunosorbent assay, WB, alkaline phosphatase, and alizarin red staining.
RESULTS: The gene and protein expression levels of SMURF1 in PDLSCs increased following LPS induction (p < 0.001); cell viability was decreased (p < 0.001), TRAF4 expression was decreased (p < 0.001), and cell-mineralized nodules were inhibited. Inhibition of SMURF1 expression increased PDLSCs activity and TRAF4 expression levels (p < 0.001), increased the number of cell-mineralized nodules, and enhanced cellular osteogenic capacity (p < 0.001).
CONCLUSIONS: SMURF1 regulates LPS-stimulated injury and improves the capacity for osteogenic differentiation in PDLSCs by downregulating the expression of TRAF4.