PMID: 11901316Mar 20, 2002Paper

Slow channel calcium inhibition blocks proinflammatory gene signaling and reduces macrophage responsiveness

The Journal of Trauma
Joseph CuschieriRonald V Maier

Abstract

This study investigates the possible intracellular mechanisms responsible for calcium antagonist protection in tissue-fixed macrophages, a central modulator of the proinflammatory phenotype. Rabbit alveolar macrophages were exposed to lipopolysaccharide in the presence of different specific calcium antagonists. Cellular and nuclear protein were extracted and analyzed by Western blot for the phosphorylated forms of PYK2, ERK 1/2, and p38, and nuclear translocation of NF-kappaB and AP-1. Tumor necrosis factor-alpha (TNF-alpha) expression was measured by an L929 bioassay on cellular supernatants. Statistical analysis was performed by unpaired Student's t tests. Cells pretreated with 100 to 500 micromol/L of diltiazem or 50 to 100 micromol/L of verapamil, both slow channel calcium blockers, led to dose-dependent reductions in lipopolysaccharide-induced PYK2 and ERK 1/2 phosphorylation, and nuclear translocation of AP-1 when compared with controls (p < 0.05). Neither inhibitor had any significant effect on p38 or NF-kappaB translocation. EGTA an extracellular calcium chelator, had no significant effect on any intracellular process studied. A dose-dependent reduction in TNF-alpha production was demonstrated with diltiazem and verapam...Continue Reading

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Citations

Apr 3, 2010·Inflammation Research : Official Journal of the European Histamine Research Society ... [et Al.]·Katharina BergerThomas Volk
Mar 27, 2010·Cell Biology and Toxicology·Flavia Mazzoli-RochaWalter Araújo Zin
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