1α,25-Dihydroxyvitamin D3 inhibits vascular cellular adhesion molecule-1 expression and interleukin-8 production in human coronary arterial endothelial cells

2012 ◽  
Vol 132 (3-5) ◽  
pp. 290-294 ◽  
Author(s):  
Keiko Kudo ◽  
Shunji Hasegawa ◽  
Yasuo Suzuki ◽  
Reiji Hirano ◽  
Hiroyuki Wakiguchi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Cellular Adhesion ◽  
Interleukin 8 ◽  
Dihydroxyvitamin D3 ◽  
Cellular Adhesion Molecule ◽  
Arterial Endothelial Cells

scholarly journals The Hinge-Helix 1 Region of Peroxisome Proliferator-Activated Receptor γ1 (PPARγ1) Mediates Interaction with Extracellular Signal-Regulated Kinase 5 and PPARγ1 Transcriptional Activation: Involvement in Flow-Induced PPARγ Activation in Endothelial Cells

2004 ◽  
Vol 24 (19) ◽  
pp. 8691-8704 ◽  
Author(s):  
Masashi Akaike ◽  
Wenyi Che ◽  
Nicole-Lerner Marmarosh ◽  
Shinsuke Ohta ◽  
Masaki Osawa ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Critical Role ◽  
Physiological Role ◽  
Cellular Adhesion ◽  
Dominant Negative ◽  
Peroxisome Proliferator ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Cellular Adhesion Molecule

ABSTRACT Peroxisome proliferator-activated receptors (PPAR) are ligand-activated transcription factors that form a subfamily of the nuclear receptor gene family. Since both flow and PPARγ have atheroprotective effects and extracellular signal-regulated kinase 5 (ERK5) kinase activity is significantly increased by flow, we investigated whether ERK5 kinase regulates PPARγ activity. We found that activation of ERK5 induced PPARγ1 activation in endothelial cells (ECs). However, we could not detect PPARγ phosphorylation by incubation with activated ERK5 in vitro, in contrast to ERK1/2 and JNK, suggesting a role for ERK5 as a scaffold. Endogenous PPARγ1 was coimmunoprecipitated with endogenous ERK5 in ECs. By mammalian two-hybrid analysis, we found that PPARγ1 associated with ERK5a at the hinge-helix 1 region of PPARγ1. Expressing a hinge-helix 1 region PPARγ1 fragment disrupted the ERK5a-PPARγ1 interaction, suggesting a critical role for hinge-helix 1 region of PPARγ in the ERK5-PPARγ interaction. Flow increased ERK5 and PPARγ1 activation, and the hinge-helix 1 region of the PPARγ1 fragment and dominant negative MEK5β significantly reduced flow-induced PPARγ activation. The dominant negative MEK5β also prevented flow-mediated inhibition of tumor necrosis factor alpha-mediated NF-κB activation and adhesion molecule expression, including vascular cellular adhesion molecule 1 and E-selectin, indicating a physiological role for ERK5 and PPARγ activation in flow-mediated antiinflammatory effects. We also found that ERK5 kinase activation was required, likely by inducing a conformational change in the NH2-terminal region of ERK5 that prevented association of ERK5 and PPARγ1. Furthermore, association of ERK5a and PPARγ1 disrupted the interaction of SMRT and PPARγ1, thereby inducing PPARγ activation. These data suggest that ERK5 mediates flow- and ligand-induced PPARγ activation via the interaction of ERK5 with the hinge-helix 1 region of PPARγ.

Stimulation of p-selectin, e-selectin and cellular adhesion molecule expression by H. pylori in endothelial cells mediates increased neutrophil adhesion

2001 ◽  
Vol 120 (5) ◽  
pp. A670
Author(s):  
Michael F. Byrne ◽  
Paul A. Corcoran ◽  
Katherine M. Sheehan ◽  
John C. Atherton ◽  
Desmond J. Fitzgerald ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Cellular Adhesion ◽  
Neutrophil Adhesion ◽  
Adhesion Molecule Expression ◽  
Cellular Adhesion Molecule ◽  
H Pylori ◽  
Stimulation Of

Abstract 61: Anti-inflammatory Effect Of Resveratrol In Human Coronary Arterial Endothelial Cells Via Autophagy: Implication For The Treatment Of Kawasaki Disease

Circulation ◽  
2015 ◽  
Vol 131 (suppl_2) ◽  
Author(s):  
Fu-Chen Huang Huang ◽  
Ho-Chang Kuo ◽  
Hong-Ren Yu
Keyword(s):  
Endothelial Cells ◽  
Kawasaki Disease ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Cellular Adhesion ◽  
Tnf Alpha ◽  
Coronary Aneurysms ◽  
Cellular Adhesion Molecule ◽  
Increased Risk ◽  
Anti Inflammatory

Kawasaki disease (KD) is an acute febrile vasculitis of childhood and is the leading cause of acquired heart disease in children in the developed world. If untreated, KD can result in coronary aneurysms in 25% of patients, who are at risk of myocardial infarction, sudden death, and congestive heart failure. Despite the success, 10-20% of children will have persistent or recrudescent fever after their first infusion of IVIG. These patients are at increased risk of developing coronary artery abnormalities. Additional therapies should be explored to decrease the incidence of coronary arteritis complication and improve the prognosis in Kawasaki disease. Induced autophagy with resveratrol confers cardioprotection during ischemia and reperfusion in rats. KD is associated with elevated production of inflammatory cytokines, causing damage to the coronary arteries. Serum TNF-alpha levels are elevated in KD, which was supposed to activate the endothelial cells. As a result, adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1) and vascular cellular adhesion molecule-1(VCAM-1) are expressed in the endothelial cells, and leucocytes adhere firmly to endothelial cells. The leucocytes then damage the endothelial cells and smooth muscle cells and cause vasculitis. In this study, we examined the anti-inflammatory effects of resveratrol on TNF-alpha-induced adhesion molecule expression (VCAM-1 and ICAM-1) and cytokine production (interleukin (IL)-1beta, IL-6 and IL-8) in HCAECs. Pretreatment with resveratrol significantly inhibited TNF-alpha-induced adhesion molecules and cytokines production in HCAECs via the activation of autophagy. Our results suggest that adjunctive resveratrol therapy may modulate the inflammatory response during KD vasculitis and explore the role of autophagy in the pathogenesis of the complication and the promising therapy.

scholarly journals Protective Effects of Resveratrol on TNF-α-Induced Endothelial Cytotoxicity in Baboon Femoral Arterial Endothelial Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Juan Xiao ◽  
Jun Song ◽  
Vida Hodara ◽  
Allen Ford ◽  
Xing Li Wang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Critical Role ◽  
Primary Cultures ◽  
Vascular Diseases ◽  
Cellular Adhesion ◽  
Inflammatory Factors ◽  
High Dose ◽  
Protective Effects ◽  
Cellular Adhesion Molecule ◽  
Arterial Endothelial Cells

Endothelial injury induced by inflammatory factors plays a critical role in the pathogenesis of cardiovascular disease. Endothelial cell (EC) apoptosis, proliferation, migration, and cellular adhesion molecule (CAM) expression contribute to the development of atherosclerosis. We investigated the effects of resveratrol (0.1–100 μM) on the proliferation, migration, and CAM expression of primary cultures of baboon arterial endothelial cells (BAECs). In addition, we tested its effects under normal conditions as well as under inflammatory conditions induced by tumour necrosis factor-α(TNF-α) administered either by cotreatment, pretreatment, or posttreatment. Immunocytochemistry, MTT, wound-healing, and flow cytometry assays were performed. The resveratrol treatment significantly enhanced BAEC proliferation and attenuated TNF-α-induced impairment of proliferation at the optimal doses of 1–50 µM. Resveratrol at a high dose (100 μM) and TNF-αimpaired BAEC migration, while low doses of resveratrol (1–50 μM) attenuated TNF-α-induced impairment of BAEC migration. Moreover, resveratrol inhibited TNF-α-induced ICAM-1 and VCAM-1 expression. Taken together, our results suggest that the resveratrol protects BAECs after inflammatory stimulation as well as ameliorates inflammatory effects at low concentrations. Consequently, resveratrol should be considered as a candidate drug for the prevention and treatment of inflammatory vascular diseases.

Sign in / Sign up

Export Citation Format

Share Document