PMID- 19285037
OWN - NLM
STAT- MEDLINE
DCOM- 20090506
LR  - 20190412
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 382
IP  - 2
DP  - 2009 May 1
TI  - Extracellular ATP-induced nuclear Ca2+ transient is mediated by inositol 
      1,4,5-trisphosphate receptors in mouse pancreatic beta-cells.
PG  - 381-4
LID - 10.1016/j.bbrc.2009.03.030 [doi]
AB  - Extracellular ATP (eATP) induces an intracellular Ca(2+) transient by activating 
      phospholipase C (PLC)-associated P2X4 purinergic receptors, leading to production 
      of inositol 1,4,5-trisphosphate (IP3) and subsequent Ca(2+) release from 
      intracellular stores in mouse pancreatic beta-cells. Using laser scanning 
      confocal microscopy, Ca(2+) indicator fluo-4 AM, and the cell permeable nuclear 
      indicator Hoechst 33342, we examined the properties of eATP-induced Ca(2+) 
      release in pancreatic beta-cell nuclei. eATP induced a higher nuclear Ca(2+) 
      transient in pancreatic beta-cell nuclei than in the cytosol. After pretreatment 
      with thapsigargin (TG), an inhibitor of sarco-endoplasmic reticulum Ca(2+)-ATPase 
      (SERCA) pumps, the amplitude of eATP-induced Ca(2+) transients in the nucleus was 
      still much higher than those in the cytosol. This effect of eATP was not altered 
      by inhibition of either the plasma membrane Ca(2+)-ATPase (PMCA) or the plasma 
      membrane Na(+)/Ca(2+) exchanger (NCX) by LaCl(3) or by replacement of Na(+) with 
      N-Methyl-Glucosamine. eATP-induced nuclear Ca(2+) transients were abolished by a 
      cell-permeable IP3R inhibitor, 2-aminoethoxydiphenyl borate (2-APB), but were not 
      blocked by the ryanodine receptor (RyR) antagonist ryanodine. Immunofluorescence 
      studies showed that IP3Rs are expressed on the nuclear envelope of pancreatic 
      beta-cells. These results indicate that eATP triggers nuclear Ca(2+) transients 
      by mobilizing a nuclear Ca(2+) store via nuclear IP3Rs.
FAU - Chen, Zheng
AU  - Chen Z
AD  - National Laboratory of Biomacromolecules, Institute of Biophysics of Chinese 
      Academy of Sciences, Beijing, China.
FAU - Li, Zhengzheng
AU  - Li Z
FAU - Peng, Gong
AU  - Peng G
FAU - Chen, Xiaoli
AU  - Chen X
FAU - Yin, Wenxuan
AU  - Yin W
FAU - Kotlikoff, Michael I
AU  - Kotlikoff MI
FAU - Yuan, Zeng-Qiang
AU  - Yuan ZQ
FAU - Ji, Guangju
AU  - Ji G
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090311
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Atp2a1 protein, mouse)
RN  - 0 (Benzimidazoles)
RN  - 0 (Fluorescent Dyes)
RN  - 0 (Inositol 1,4,5-Trisphosphate Receptors)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - EC 3.6.3.8 (Plasma Membrane Calcium-Transporting ATPases)
RN  - EC 3.6.3.8 (Sarcoplasmic Reticulum Calcium-Transporting ATPases)
RN  - EC 7.2.2.10 (Atp2b1 protein, mouse)
RN  - P976261J69 (bisbenzimide ethoxide trihydrochloride)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Adenosine Triphosphate/*metabolism/pharmacology
MH  - Animals
MH  - Benzimidazoles/metabolism
MH  - Calcium/*metabolism
MH  - *Calcium Signaling
MH  - Cell Nucleus/*metabolism
MH  - Fluorescent Dyes/metabolism
MH  - Inositol 1,4,5-Trisphosphate Receptors/*metabolism
MH  - Insulin-Secreting Cells/drug effects/*metabolism
MH  - Mice
MH  - Plasma Membrane Calcium-Transporting ATPases/metabolism
MH  - Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism
EDAT- 2009/03/17 09:00
MHDA- 2009/05/07 09:00
CRDT- 2009/03/17 09:00
PHST- 2009/02/25 00:00 [received]
PHST- 2009/03/06 00:00 [accepted]
PHST- 2009/03/17 09:00 [entrez]
PHST- 2009/03/17 09:00 [pubmed]
PHST- 2009/05/07 09:00 [medline]
AID - S0006-291X(09)00491-4 [pii]
AID - 10.1016/j.bbrc.2009.03.030 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2009 May 1;382(2):381-4. doi: 
      10.1016/j.bbrc.2009.03.030. Epub 2009 Mar 11.