PMID- 30416166
OWN - NLM
STAT- MEDLINE
DCOM- 20190415
LR  - 20190415
IS  - 1347-5215 (Electronic)
IS  - 0918-6158 (Linking)
VI  - 42
IP  - 1
DP  - 2019 Jan 1
TI  - L-Type Calcium Channel-Mediated Zinc Wave Is Involved in the Regulation of IL-6 
      by Stimulating Non-IgE with LPS and IL-33 in Mast Cells and Dendritic Cells.
PG  - 87-93
LID - 10.1248/bpb.b18-00565 [doi]
AB  - The trace element zinc is essential for the immune system, and its dysregulation 
      and deficiency results in impaired immune function. Recent studies have shown 
      that zinc can behave as an intracellular signaling molecule in immune cells. We 
      have previously demonstrated that L-type calcium channel (LTCC) is involved in 
      the regulation of zinc signaling, Zinc wave and cytokine production by 
      stimulating Fc epsilon receptor for immunoglobulin E (IgE) in mast cells. 
      However, it is not known whether LTCC-mediated Zinc wave is required for cytokine 
      production by stimulation of toll-like receptors and cytokine receptors in mast 
      cells. Here we report that stimulation of toll-like receptors and cytokine 
      receptors can induce Zinc wave in mast cells and regulate the expression of 
      cytokine genes. The LTCC antagonist nicardipine inhibited lipopolysaccharide 
      (LPS)- and interleukin-33 (IL-33)-mediated Zinc wave and the induction of 
      cytokine genes such as IL-6. Consistent with these results, the zinc chelator 
      N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN) also inhibited LPS- and 
      IL-33-induced cytokine gene expression. Furthermore, LPS induced Zinc wave not 
      only in mast cells but also in dendritic cells. Together, these observations show 
      that Zinc wave is activated by various stimuli and is linked to cytokine gene 
      induction in immune cells.
FAU - Uchida, Ryota
AU  - Uchida R
AD  - Laboratory of Immune Regulation, Graduate School of Pharmaceutical Sciences, 
      Suzuka University of Medical Science.
FAU - Xiang, Huihui
AU  - Xiang H
AD  - Division of Functional Immunology, Institute for Genetic Medicine, Hokkaido 
      University.
FAU - Arai, Hiroya
AU  - Arai H
AD  - Laboratory of Immune Regulation, Faculty of Pharmaceutical Sciences, Suzuka 
      University of Medical Science.
FAU - Kitamura, Hidemitsu
AU  - Kitamura H
AD  - Division of Functional Immunology, Institute for Genetic Medicine, Hokkaido 
      University.
FAU - Nishida, Keigo
AU  - Nishida K
AD  - Laboratory of Immune Regulation, Graduate School of Pharmaceutical Sciences, 
      Suzuka University of Medical Science.
AD  - Laboratory of Immune Regulation, Faculty of Pharmaceutical Sciences, Suzuka 
      University of Medical Science.
LA  - eng
PT  - Journal Article
DEP - 20181110
PL  - Japan
TA  - Biol Pharm Bull
JT  - Biological & pharmaceutical bulletin
JID - 9311984
RN  - 0 (Calcium Channels, L-Type)
RN  - 0 (Il33 protein, mouse)
RN  - 0 (Interleukin-33)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipopolysaccharides)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - J41CSQ7QDS (Zinc)
SB  - IM
MH  - Animals
MH  - CHO Cells
MH  - Calcium Channels, L-Type/*physiology
MH  - Cells, Cultured
MH  - Cricetinae
MH  - Cricetulus
MH  - Dendritic Cells/drug effects/*metabolism
MH  - Immunoglobulin E/metabolism
MH  - Interleukin-33/*toxicity
MH  - Interleukin-6/*physiology
MH  - Lipopolysaccharides/toxicity
MH  - Mast Cells/drug effects/*metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Zinc/*metabolism
OTO - NOTNLM
OT  - cytokine
OT  - dendritic cell
OT  - lipopolysaccharide (LPS)
OT  - mast cell
OT  - nuclear factor-kappaB (NF-kappaB)
OT  - zinc signaling
EDAT- 2018/11/13 06:00
MHDA- 2019/04/16 06:00
CRDT- 2018/11/13 06:00
PHST- 2018/11/13 06:00 [pubmed]
PHST- 2019/04/16 06:00 [medline]
PHST- 2018/11/13 06:00 [entrez]
AID - 10.1248/bpb.b18-00565 [doi]
PST - ppublish
SO  - Biol Pharm Bull. 2019 Jan 1;42(1):87-93. doi: 10.1248/bpb.b18-00565. Epub 2018 
      Nov 10.