PMID- 28458279
OWN - NLM
STAT- MEDLINE
DCOM- 20170810
LR  - 20171017
IS  - 1347-5231 (Electronic)
IS  - 0031-6903 (Linking)
VI  - 137
IP  - 5
DP  - 2017
TI  - [Regulatory Mechanism of Mast Cell Activation by Zinc Signaling].
PG  - 495-501
LID - 10.1248/yakushi.16-00239-1 [doi]
AB  - Mast cells are hematopoietic-lineage cells that participate in immunoglobulin E 
      (IgE)-associated immune responses, including allergic reactions and parasite 
      resistance. Recent studies have shown that zinc (Zn) ion can behave as an 
      intracellular signaling molecule and that Zn is involved in mast cell activation. 
      We demonstrated that mast cells stimulated through the high-affinity IgE receptor 
      (FcepsilonRI) rapidly release intracellular Zn from the endoplasmic reticulum (ER), and 
      we named this phenomenon the "Zn wave". Furthermore, we found that the L-type 
      calcium channel (LTCC) is the gatekeeper for the Zn wave. LTCC antagonists 
      inhibited the Zn wave, and an agonist was sufficient to induce it. Notably, LTCC 
      was mainly localized to the ER rather than to the plasma membrane in mast cells, 
      and the Zn wave was impaired by LTCC knockdown. We also found that the 
      LTCC-mediated Zn wave positively controlled inflammatory cytokine gene induction 
      by enhancing the DNA-binding activity of nuclear factor-kappa B (NF-kappaB). These 
      findings indicated that the LTCC has a novel function as a gatekeeper for the Zn 
      wave, which is involved in regulating NF-kappaB signaling. In this review, we 
      describe our current understanding of Zn signaling, especially with regard to the 
      Zn wave and the role of Zn signaling in mast cells.
FAU - Nishida, Keigo
AU  - Nishida K
AD  - Laboratory of Immune Regulation, Graduate School of Pharmaceutical Sciences, 
      Suzuka University of Medical Science.
FAU - Uchida, Ryota
AU  - Uchida R
AD  - Laboratory of Immune Regulation, Graduate School of Pharmaceutical Sciences, 
      Suzuka University of Medical Science.
LA  - jpn
PT  - Journal Article
PT  - Review
PL  - Japan
TA  - Yakugaku Zasshi
JT  - Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan
JID - 0413613
RN  - 0 (Calcium Channels, L-Type)
RN  - 0 (Cytokines)
RN  - 0 (Inflammation Mediators)
RN  - 0 (NF-kappa B)
RN  - 0 (Receptors, IgE)
RN  - 9007-49-2 (DNA)
RN  - J41CSQ7QDS (Zinc)
SB  - IM
MH  - Animals
MH  - Calcium Channels, L-Type/physiology
MH  - Cytokines
MH  - DNA/metabolism
MH  - Endoplasmic Reticulum/metabolism
MH  - Humans
MH  - Inflammation Mediators
MH  - Mast Cells/cytology/*immunology/*metabolism
MH  - Mice
MH  - NF-kappa B/metabolism
MH  - Protein Binding
MH  - Receptors, IgE/physiology
MH  - Signal Transduction/*physiology
MH  - Transcriptional Activation
MH  - Zinc/*metabolism/*physiology
OTO - NOTNLM
OT  - L-type calcium channel
OT  - cytokine
OT  - mast cell
OT  - zinc
EDAT- 2017/05/02 06:00
MHDA- 2017/08/11 06:00
CRDT- 2017/05/02 06:00
PHST- 2017/05/02 06:00 [entrez]
PHST- 2017/05/02 06:00 [pubmed]
PHST- 2017/08/11 06:00 [medline]
AID - 10.1248/yakushi.16-00239-1 [doi]
PST - ppublish
SO  - Yakugaku Zasshi. 2017;137(5):495-501. doi: 10.1248/yakushi.16-00239-1.