212 research outputs found
Influence of Components Deposition Order on Silver Species Formation in Bimetallic Ag-Fe System Supported on Mordenite
Effect of the preparation method on the catalytic properties of copper-containing zeolite Y applied for NH3-SCR-DeNO(x)
Characterization and possible hazard of an atypical asbestiform sepiolite associated with aliphatic hydrocarbons from Sassello (Ligurian Apennines, Italy)
Evidence of Mixed-Ligand Complexes in Cu−CHA by Reaction of Cu Nitrates with NO/NH3 at Low Temperature
In Situ Investigation of the Deactivation Mechanism in Ni-ZSM5 During Ethylene Oligomerization
Uptake and intracellular distribution of different types of nanoparticles in primary human myoblasts and myotubes
The impact of reaction conditions and material composition on the stepwise methane to methanol conversion over Cu-MOR: An operando XAS study
Dynamic CuII/CuI speciation in Cu-CHA catalysts by in situ Diffuse Reflectance UV–vis-NIR spectroscopy
Statins inhibit C-reactive protein-induced chemokine secretion, ICAM-1 upregulation and chemotaxis in adherent human monocytes
Objectives. We have recently shown that CRP induces chemokine secretion and adhesion molecule up-regulation in human primary monocytes cultured in adherence. Given the increasing evidence on direct immunomodulatory properties of statins, we investigated their possible anti-inflammatory role on CRP-treated human monocytes. Methods. Monocytes were isolated by Ficoll-Percoll gradients and cultured in adherence to polystyrene. Chemokine secretion and adhesion molecule expression were detected by ELISA and flow cytometry. Migration assays were performed in modified Boyden chambers. Intracellular kinase activation was assessed by western blot. Results. Treatment with simvastatin or atorvastatin decreased CRP-induced release of CCL2, CCL3 and CCL4. In addition, both statins reduced CRP-induced intercellular adhesion molecule (ICAM-1) up-regulation, but had no effects on CD11b and CD18. Treatments with 1 μM simvastatin or atorvastatin significantly inhibited monocyte migration in response to CRP. CD32 and CD64 (CRP receptors) expression on monocytes was not affected by statins. Statin-induced inhibition of CRP-mediated chemokine secretion, ICAM-1 up-regulation and migration occurred through the inhibition of extracellular signal-regulated kinase (ERK) 1/2. Treatment with l-mevalonate or farnesylpyrophosphate, but not geranylgeranyl-pyrophosphate reversed the statin-induced effect on CRP-mediated functions and ERK 1/2 phosphorylation, confirming that statins blocked CRP-induced ERK 1/2 phosphorylation through the inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. Conclusions. Statins inhibited CRP-induced chemokine secretion, ICAM-1 up-regulation and migration in human adherent monocytes, through the inhibition of HMG-CoA reductase-ERK 1/2 pathway. This pathway could represent a very promising target to reduce CRP-induced activities in monocyte-mediated diseases, such as atherosclerosis or R
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