TNF-α and LPS activate angiogenesis via VEGF and SIRT1 signalling in human dental pulp cells
Autor: | Eun-Cheol Kim, Sun-Ju Lee, Young-Sick Kim, Soo-Kyung Kang, Seon-Pyo Hong, Mee-Ran Shin |
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Rok vydání: | 2014 |
Předmět: |
Lipopolysaccharides
Vascular Endothelial Growth Factor A MAPK/ERK pathway MAP Kinase Signaling System Angiogenesis p38 mitogen-activated protein kinases Blotting Western Neovascularization Physiologic Endothelial Growth Factors Naphthols Matrix metalloproteinase Biology Real-Time Polymerase Chain Reaction Peptides Cyclic chemistry.chemical_compound Sirtuin 1 Downregulation and upregulation Cell Movement Humans Phosphorylation General Dentistry Protein kinase B Cells Cultured Dental Pulp Adaptor Proteins Signal Transducing Tube formation Tumor Necrosis Factor-alpha JNK Mitogen-Activated Protein Kinases Up-Regulation Vascular endothelial growth factor chemistry Benzamides Immunology Cancer research Apoptosis Regulatory Proteins Signal Transduction |
Zdroj: | International Endodontic Journal. 48:705-716 |
ISSN: | 0143-2885 |
Popis: | Aim To assess whether SIRT1 and VEGF are responsible for tumour necrosis factor-α (TNF-α) and lipopolysaccharide (LPS)-induced angiogenesis and to examine the molecular mechanism(s) of action in human dental pulp cells (HDPCs). Methodology Immortalized HDPCs obtained from Prof. Takashi Takata (Hiroshima University, Japan) were treated with LPS (1 μg mL−1) and TNF-α (10 ng mL−1) for 24 h. mRNA and protein levels were examined by RT-PCR and Western blotting, respectively. Migration and tube formation were examined in human umbilical vein endothelial cells (HUVECs). The data were analysed by one-way anova. Statistical analysis was performed at α = 0.05. Results LPS and TNF-α upregulated VEGF and SIRT1 mRNA and protein levels. Inhibition of SIRT1 activity by sirtinol and SIRT1 siRNA or inhibition of the VEGF receptor by CBO-P11 significantly attenuated LPS + TNF-α-stimulated MMPs production in HDPCs, as well as migration and tube formation in HUVECs (P |
Databáze: | OpenAIRE |
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