Regulation of Vascular Cell Adhesion Molecule-1 in Dental Pulp Cells by Interleukin-1β: The Role of Prostanoids

Chang, Mei Chi; Lin, Li‐Deh; Chang, Jenny Zwei-Ching; Huang, Chiung Fang; Chuang, Fu Hsiung; Lee, Jang‐Jaer; Jeng, Po Yuan; Wang, Tong-Mei; Jeng, Jiiang‐Huei

doi:10.1016/j.joen.2012.02.030

Cited by 21 publications

(11 citation statements)

References 32 publications

(56 reference statements)

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“…When the combined action of BAY11-7082 and LTA was up to 24 hours, mRNA and protein expression of IL-1b was lower than that of the LTA group, but both were higher than that of the negative control group. This may be because IL-1b was the product of various inflammatory pathways (33,34).…”

Section: Discussionmentioning

confidence: 99%

Enterococcus faecalis Lipoteichoic Acid–induced NLRP3 Inflammasome via the Activation of the Nuclear Factor Kappa B Pathway

Wang

Jin

et al. 2016

Journal of Endodontics

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Section: Discussionmentioning

confidence: 99%

Enterococcus faecalis Lipoteichoic Acid–induced NLRP3 Inflammasome via the Activation of the Nuclear Factor Kappa B Pathway

Wang

Jin

et al. 2016

Journal of Endodontics

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“…Testosterone induces VCAM expression in cultured VSMC (Supplementary Figure S3). Reports in the literature have shown that non-specific COX inhibitors are not effective in blocking IL1β-induced VCAM-1 expression in primary dental pulp cells [32] and human umbilical vein endothelial cells (HUVECs) [33]. Reports in the literature have shown that non-specific COX inhibitors are not effective in blocking IL1β-induced VCAM-1 expression in primary dental pulp cells [32] and human umbilical vein endothelial cells (HUVECs) [33].…”

Section: Discussionmentioning

confidence: 99%

Testosterone induces leucocyte migration by NADPH oxidase-driven ROS- and COX2-dependent mechanisms

et al. 2015

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The mechanisms whereby testosterone increases cardiovascular risk are not clarified. However, oxidative stress and inflammation seem to be determinants. Herein, we sought to determine whether exogenous testosterone, at physiological levels, induces leucocyte migration, a central feature in immune and inflammatory responses and the mediating mechanisms. We hypothesized that testosterone induces leucocyte migration via NADPH oxidase (NADPHox)-driven reactive oxygen species (ROS) and cyclooxygenase (COX)-dependent mechanisms. Sixteen-week-old Wistar rats received an intraperitoneal injection (5 ml) of either testosterone (10(-7) mol/l) or saline. Rats were pre-treated with 5 ml of sodium salicylate (SS, non-selective COX inhibitor, 1.25 × 10(-3) mol/l, 1 h prior to testosterone or saline), flutamide (androgen receptor antagonist, 10(-5) mol/l), apocynin (NADPHox inhibitor, 3 × 10(-4) mol/l), N-[2-Cyclohexyloxy-4-nitrophenyl]methanesulfonamide (NS398, COX2 inhibitor, 10(-4) mol/l) or saline, 4 h before testosterone or saline administration. Leucocyte migration was assessed 24 h after testosterone administration by intravital microscopy of the mesenteric bed. Serum levels of testosterone were measured by radioimmunoassay. NADPHox activity was assessed in membrane fractions of the mesenteric bed by dihydroethidium (DHE) fluorescence and in isolated vascular smooth muscle cells (VSMC) by HPLC. NADPHox subunits and VCAM (vascular cell adhesion molecule) expression were determined by immunoblotting. Testosterone administration did not change serum levels of endogenous testosterone, but increased venular leucocyte migration to the adventia, NADPHox activity and expression (P < 0.05). These effects were blocked by flutamide. SS inhibited testosterone-induced leucocyte migration (P<0.05). Apocynin and NS398 abolished testosterone-induced leucocyte migration and NADPHox activity (P<0.05). Testosterone induces leucocyte migration via NADPHox- and COX2-dependent mechanisms and may contribute to inflammatory processes and oxidative stress in the vasculature potentially increasing cardiovascular risk.

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“…The IL-1 family, which includes IL-1α and IL-1β, exhibits strong pro-inflammatory activities and plays a major role in host responses to exogenous and endogenous noxious stimuli (Gabay et al, 2010). IL-1 induces the expression of adhesion molecules on endothelial cells and elicits stromal cells to release chemokines that promote the recruitment of inflammatory cells at the inflammation site (Dinarello, 1996; Chang et al, 2012; Hu et al, 2012). Such inflammation occurs significantly in cases of comorbidity and might contribute to the increased risk of developing cardiovascular accidents observed in these patients (Carpagnano et al, 2010).…”

Section: Mediators Of Inflammationmentioning

confidence: 99%

Apoptotic cell: linkage of inflammation and wound healing

2014

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We consider that from the wound to the healing process, the physiology point key to linkage of the process is still unclear. The process from inflammation to the wound healing is divided into three phases: (1) inflammation process, (2) tissue formation, and (3) tissue remodeling. The inflammation program includes cell produced related factors and immune cells infiltration. We thought the inflammation factors that may be also involved in the followed healing process. But the question is “what kind of factor is the major key involved in the end of the inflammation then to initiate the healing.” We suspect that the apoptosis of immune cell may be the major key to end of inflammation and to initiate the healing.

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Regulation of Vascular Cell Adhesion Molecule-1 in Dental Pulp Cells by Interleukin-1β: The Role of Prostanoids

Cited by 21 publications

References 32 publications

Enterococcus faecalis Lipoteichoic Acid–induced NLRP3 Inflammasome via the Activation of the Nuclear Factor Kappa B Pathway

Enterococcus faecalis Lipoteichoic Acid–induced NLRP3 Inflammasome via the Activation of the Nuclear Factor Kappa B Pathway

Testosterone induces leucocyte migration by NADPH oxidase-driven ROS- and COX2-dependent mechanisms

Apoptotic cell: linkage of inflammation and wound healing

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