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231223s2008 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2008.08.001
|2 doi
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|a pubmed24n0608.xml
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|a (DE-627)NLM182417069
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|a (NLM)18790672
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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|a Lu, Ming-Chi
|e verfasserin
|4 aut
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|a Nifedipine suppresses Th1/Th2 cytokine production and increased apoptosis of anti-CD3 + anti-CD28-activated mononuclear cells from patients with systemic lupus erythematosus via calcineurin pathway
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|c 2008
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 04.12.2008
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|a Date Revised 16.11.2017
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Increased Ca(2+) 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 Ca(2+) 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 microM nifedipine could suppress SLE-MNC IFN-gamma secretion but 10 microM nifedipine was required for suppressing that of normal MNC. IL-10 secretion by both SLE-MNC and normal MNC was suppressed by 1 microM nifedipine. However, high dose of nifedipine (50 microM) 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 Ca(2+) channel blocker-mediated apoptosis and cytokine suppression. We proposed that L-type Ca(2+) channel blocker maybe a potential medication for controlling SLE
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a Adaptor Proteins, Signal Transducing
|2 NLM
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|a CABIN1 protein, human
|2 NLM
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|a CD28 Antigens
|2 NLM
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|a CD3 Complex
|2 NLM
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|a Calcium Channel Blockers
|2 NLM
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|a Calcium Channels, L-Type
|2 NLM
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|a Cytokines
|2 NLM
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|a FASLG protein, human
|2 NLM
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|a Fas Ligand Protein
|2 NLM
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|a NFATC Transcription Factors
|2 NLM
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|a NFATC1 protein, human
|2 NLM
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|a Interleukin-10
|2 NLM
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|a 130068-27-8
|2 NLM
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|a Interferon-gamma
|2 NLM
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|a 82115-62-6
|2 NLM
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|a Calcineurin
|2 NLM
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|a EC 3.1.3.16
|2 NLM
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|a Phosphoric Monoester Hydrolases
|2 NLM
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|a EC 3.1.3.2
|2 NLM
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|a Nifedipine
|2 NLM
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|a I9ZF7L6G2L
|2 NLM
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1 |
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|a Lai, Ning-Sheng
|e verfasserin
|4 aut
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1 |
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|a Yu, Hui-Chun
|e verfasserin
|4 aut
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|a Hsieh, Song-Chou
|e verfasserin
|4 aut
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|a Tung, Chien-Hsueh
|e verfasserin
|4 aut
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|a Yu, Chia-Li
|e verfasserin
|4 aut
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 129(2008), 3 vom: 10. Dez., Seite 462-70
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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|g volume:129
|g year:2008
|g number:3
|g day:10
|g month:12
|g pages:462-70
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|u http://dx.doi.org/10.1016/j.clim.2008.08.001
|3 Volltext
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|a GBV_ILN_350
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|a AR
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|d 129
|j 2008
|e 3
|b 10
|c 12
|h 462-70
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