Your browser doesn't support javascript.
loading
TIFA contributes to periodontitis in diabetic mice via activating the NF­κB signaling pathway.
Guo, Xiaoqian; Qiao, Guangwei; Wang, Jingjiao; Yang, Changyi; Zhao, Min; Zhang, Qian; Wan, Yingbiao.
Afiliación
  • Guo X; Department of Periodontology, General Hospital of Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
  • Qiao G; Department of Oral and Maxillofacial Surgery, General Hospital of Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
  • Wang J; Department of Periodontology, General Hospital of Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
  • Yang C; Department of Periodontology, General Hospital of Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
  • Zhao M; Department of Periodontology, General Hospital of Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
  • Zhang Q; Department of Periodontology, General Hospital of Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
  • Wan Y; Department of Prosthodontics and Oral Implantology, General Hospital of Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
Mol Med Rep ; 29(2)2024 02.
Article en En | MEDLINE | ID: mdl-38099344
ABSTRACT
Diabetic periodontitis (DP) refers to destruction of periodontal tissue and absorption of bone tissue in diabetic patients. Tumor necrosis factor receptor­associated factor (TRAF)­interacting protein with forkhead­associated domain (TIFA) as a crucial regulator of inflammation activates the NF­κB signaling pathway to regulate cell biological behavior. However, the function and mechanism of TIFA on DP suffer from a lack of research. In the present study, TIFA was upregulated in the periodontal tissue of a DP mouse model. In addition, the expression of TIFA in RAW264.7 cells was induced by high glucose (HG) culture and increased by lipopolysaccharide (LPS) from Porphyromonas gingivalis treatment in a time­dependent manner. Knockdown of TIFA significantly reduced the levels of inflammatory cytokines, including TNF­α, IL­6, IL­1ß and monocyte chemoattractant protein­1, in HG and LPS­induced RAW264.7 cells. The nuclear translocation of NF­κB p65 was induced by HG and LPS and was clearly suppressed by absence of TIFA. The expression of downstream factors Nod­like receptor family pyrin domain­containing 3 and apoptosis­associated speck­like protein was inhibited by silencing TIFA. Moreover, TIFA was increased by receptor activator of NF­κB (RANK) ligand (RANKL) in a concentration dependent manner. The expression of cathepsin K, MMP9 and nuclear factor of activated T cells cytoplasmic 1 was downregulated by depletion of TIFA. RANKL­induced osteoclast differentiation was inhibited by silencing of TIFA. Meanwhile, the decrease of TIFA blocked activation of the NF­κB pathway in RANKL­treated RAW264.7 cells. In conclusion, TIFA as a promoter regulates the inflammation and osteoclast differentiation via activating the NF­κB signaling pathway.
Asunto(s)
Palabras clave
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Periodontitis / Diabetes Mellitus Experimental Límite: Animals / Humans Idioma: En Revista: Mol Med Rep Año: 2024 Tipo del documento: Article Pais de publicación: Grecia
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Periodontitis / Diabetes Mellitus Experimental Límite: Animals / Humans Idioma: En Revista: Mol Med Rep Año: 2024 Tipo del documento: Article Pais de publicación: Grecia