PPARγ affects nitric oxide in human umbilical vein endothelial cells exposed to Porphyromonas gingivalis

• PPARγ was activated in HUVECs exposed to P. gingivalis.
• Activated PPARγ increased NO production in HUVECs stimulated by P. gingivalis.
• Activated PPARγ increased NO production through induced phospho-endothelial NOS expression.

ObjectivePorphyromonas gingivalis induces nitric oxide (NO) synthesis in human umbilical vein endothelial cells (HUVECs). Peroxisome proliferator-activated receptor (PPARγ) has an anti-inflammation function, and its involvement in this NO induction process requires elucidation. Here, we focused on PPARγ expression in HUVECs exposed to P. gingivalis, and investigated its effects on NO synthesis.Materials and methodsHUVECs were time-dependently stimulated by P. gingivalis W83 for 0–24 h. PPARγ expression was assessed at the mRNA and protein levels, and PPARγ activation was measured using dual-luciferase reporter assays. NO synthesis and NO synthase (NOS) expression in response to P. gingivalis were examined in HUVECs pretreated with representative PPARγ agonist (15-deoxy-Δ12,14-prostaglandin J2 10 μM) or antagonist (GW9662 10 μM). In addition, NO synthesis and NOS expression in the P. gingivalis infected and control groups were detected.ResultsThe PPARγ mRNA level in HUVECs increased after exposure to P. gingivalis for 1 h and its protein level increased at 2 h. Luciferase-induced PPARγ increased in P. gingivalis-exposed HUVECs. NO synthesis in the infected group at 4 h, and in the PPARγ-activated group at 8 h, was higher than that in controls. Inducible NOS increased in the infected and PPARγ-activated groups at 4 and 8 h. The total endothelial NOS (eNOS) and phospho-eNOS levels were lower in the infected group than controls, but did not change in the PPARγ-activated group.ConclusionsActivated PPARγ induces NO generation through the NOS pathway in HUVECs exposed to P. gingivalis.