Effect of Nicotine and Porphyromonas gingivalis Lipopolysaccharide on Endothelial Cells In Vitro

Abstract

Smoking is considered a significant risk factor for both periodontal disease and cardiovascular disease (CVD). Endothelial cells play an important role in the progression of both diseases. In the present study, we investigated in vitro the impact of nicotine on functional properties of human umbilical vein endothelial cells (HUVECs) stimulated with lipopolysaccharide (LPS) of periodontal pathogen Porphyromonas gingivalis. HUVECs were stimulated with different concentrations of nicotine (10 µM-10 mM) and/or P. gingivalis LPS. Expression levels of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin, monocyte chemoattractant protein 1, and interleukin-8 were measured on both gene and protein levels. Cell proliferation/viability, apoptosis, and migration were also investigated. Nicotine at a concentration of 10 mM significantly decreased P. gingivalis LPS-induced expression of all investigated proteins after 4 h stimulation, while lower nicotine concentrations had no significant effect on protein expression with or without P. gingivalis LPS. Proliferation/viability of HUVECs was also significantly inhibited by 10-mM nicotine but not by lower concentrations. Migration of HUVECs was significantly decreased by nicotine at concentrations of 1–10 mM. Nicotine at a concentration similar to that observed in the serum of smokers had no significant effect on the functional properties of HUVECs. However, high concentrations of nicotine, similar to that observed in the oral cavity of smokers, inhibited the inflammatory response of HUVECs. This effect of nicotine might be associated with decreased gingival bleeding indices in smoking periodontitis patients.

Tobacco‐induced suppression of the vascular response to dental plaque

“…91 Interestingly, in vitro exposure of endothelial cells to high levels of nicotine (10 mm) resulted in reduced production of the leukocyte chemoattractant, IL-8, and a suppression of endothelial migration in response to stimulation with P. gingivalis-derived LPS. 92 Such evidence is supportive of the anti-angiogenesis hypothesis.…”

Effect of enamel matrix derivative on the angiogenic behaviors of human umbilical vein endothelial cells on different titanium surfaces

“…Some previous studies showed that EMD stimulates differentiation of osteoblasts grown on moderately rough Ti surfaces 17,19) . One of these studies show that EMD promotes the proliferation and differentiation of osteoblasts an both PT and SLA surfaces, which suggest that the effect of EMD on osteoblasts does not depend on the Ti surface topography 29) .…”

“…The expression of the angiogenesis related genes intercellular adhesion molecule-1 (ICAM-1), E-selectin, endothelial protein C receptor (EPCR), von Willebrand Factor (vWF), and angopoietin-2 (Ang-2) in HUVECs was measured by quantitative polymerase chain reaction (qPCR) as described previously 13,19) )control. The statistical differences between the effects of the various titanium surfaces on the cultured cells were analyzed by one-way analysis of variance (ANOVA) for repeated measures followed by t-test.…”

Porphyromonas gingivalis Lipopolysaccharide Stimulation of Vascular Smooth Muscle Cells Activates Proliferation and Calcification

“…However, the mechanisms of this relationship have remained obscure. Studies have also indicated that Pg ‐LPS can access systemic circulation and increase the inflammatory response, leading to the breakdown of vascular cells 19 , 20 . In this study, it is identified that Pg ‐LPS is associated with VSMC calcification in vitro, which can further reveal the relationship of periodontal diseases and vascular calcification.…”

“…Studies have also indicated that Pg-LPS can access systemic circulation and increase the inflammatory response, leading to the breakdown of vascular cells. 19,20 In this study, it is identified that Pg-LPS is The doses of Pg-LPS investigated (0 to 1,000 ng/mL) were at the low end of the range used in in vitro and in vivo studies (0 to 50,000 ng/mL). 21,22 Dolan et al 23 reported that healthy individuals had blood LPS levels ‡10 pg/mL.…”