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Statins attenuate high mobility group box-1 protein induced vascular endothelial activation : a key role for
Jun Yang1, Congxin Huang, Jian Yang
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei Province, China.
Insights
Atorvastatin effectively inhibits high mobility group box-1 (HMGB1)-induced vascular endothelial activation by suppressing the Toll-like receptor 4/Nuclear factor-kappaB pathway. This finding supports statins
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Immunology
Background:
- High mobility group box-1 (HMGB1) is a proinflammatory cytokine linked to endothelial dysfunction and atherosclerosis.
- Atorvastatin, a statin, has anti-inflammatory effects beyond cholesterol reduction.
Purpose of the Study:
- To investigate if atorvastatin inhibits HMGB1-induced vascular endothelial activation.
- To elucidate the molecular mechanisms behind atorvastatin's anti-inflammatory effects.
Main Methods:
- Dose-dependent assessment of atorvastatin's effect on HMGB1-induced endothelial cell (EC) activation.
- Measurement of adhesion molecules (ICAM-1, E-selectin) and leukocyte-endothelial adhesion.
- Analysis of Toll-like receptor 4 (TLR4) expression, NF-κB translocation, and DNA binding activity.
- Use of a TLR4-specific inhibitor (CLI-095) to confirm pathway involvement.
Main Results:
- Atorvastatin significantly inhibited HMGB1-induced EC activation in a dose-dependent manner.
- Reduced expression of ICAM-1 and E-selectin, and decreased leukocyte-endothelial adhesion were observed.
- Atorvastatin suppressed HMGB1-induced TLR4 expression, NF-κB nuclear translocation, and DNA binding activity.
- These effects were consistent with findings using a TLR4-specific inhibitor.
Conclusions:
- Atorvastatin attenuates HMGB1-induced vascular endothelial activation.
- The mechanism involves inhibiting the TLR4/NF-κB signaling pathway.
- Provides evidence for statins targeting inflammatory processes in cardiovascular disease.
Abstract:
High mobility group box-1 (HMGB1) has recently been implicated as a proinflammatory cytokine that plays critical roles in endothelial dysfunction and atherosclerosis. Atorvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, exerts anti-inflammatory effects in the cardiovascular system beyond its cholesterol-lowering property. The aim of our study was to investigate whether atorvastatin inhibits HMGB1-induced vascular endothelial activation, and elucidate the underlying molecular mechanism. In this study, we found that atorvastatin, at concentrations ranging from 0.1 to 10 μM, effectively and in a dose-dependent manner inhibited HMGB1-induced endothelial cells (ECs) activation. Incubation of ECs with 10 μM atorvastatin reduced adhesion molecules (ICAM-1 and E-selectin) expression concomitant with a significant inhibition in HMGB1-stimulated leukocyte-endothelial adhesion. Further experiments showed that atorvastatin markedly suppressed HMGB1-induced Toll like receptor 4 (TLR4) expression, Nuclear factor kappaB (NF-κB) nuclear translocation and DNA binding activity in ECs. Similar effects were also observed in ECs pretreated with the TLR4- specific inhibitor CLI-095, suggesting an important role of TLR4/NF-κB pathway. These findings indicate that atorvastatin attenuates HMGB1-induced vascular endothelial activation. The underlying mechanism involves, at least in part, inhibition of TLR4/NF-κB-dependent signaling pathway, which provied the new evidence for therapeutic application of statins to target inflammatory processes in cardiovascular disease.
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