کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3258217 | 1207443 | 2008 | 9 صفحه PDF | دانلود رایگان |
Increased Ca2+ influx is found in mononuclear cells (MNC) of patients with systemic lupus erythematosus (SLE). The role of calcineurin and potential implication of calcium channel blocker to suppress the abnormal Ca2+ influx in SLE remain to be determined. In the present study, we found that the expression and phosphatase activity of calcineurin, but not calcineurin inhibitor in SLE-MNC were greater than normal MNC. Functionally, 1 μM nifedipine could suppress SLE-MNC IFN-γ secretion but 10 μM nifedipine was required for suppressing that of normal MNC. IL-10 secretion by both SLE-MNC and normal MNC was suppressed by 1 μM nifedipine. However, high dose of nifedipine (50 μM) suppressed NFATc1 activation in SLE-MNC and enhanced apoptosis of anti-CD3 + anti-CD28-activated SLE-MNC irrelevant to expression of Fas ligand. These data suggest that SLE-MNC overexpressed calcineurin and hyper-responded to L-type Ca2+ channel blocker-mediated apoptosis and cytokine suppression. We proposed that L-type Ca2+ channel blocker maybe a potential medication for controlling SLE.
Journal: Clinical Immunology - Volume 129, Issue 3, December 2008, Pages 462–470