PMID- 15193861
OWN - NLM
STAT- MEDLINE
DCOM- 20050201
LR  - 20191210
IS  - 0143-4160 (Print)
IS  - 0143-4160 (Linking)
VI  - 36
IP  - 2
DP  - 2004 Aug
TI  - Functional expression of Ca2+ signaling pathways in mouse embryonic stem cells.
PG  - 135-46
AB  - Mouse embryonic stem (mES) cells have the potential to differentiate into all 
      types of cells, but the physiological properties of undifferentiated mES cells, 
      including Ca2+ signaling systems, are not fully understood. In this study, we 
      investigated Ca2+ signaling pathways in mES cells by using confocal Ca2+ imaging 
      systems, patch clamp techniques and RT-PCR. The stimulations with ATP and 
      histamine (His) induced a transient increase of intracellular Ca2+ concentration 
      ([Ca2+]i), which were prevented by the pretreatment of 2-amino-ethoxydiphenyl 
      borate (2-APB), a blocker for inositol-1,4,5-triphosphate receptors (InsP3Rs). 
      The application of caffeine (Caff) or ryanodine (Ry) did not change [Ca2+]i. When 
      stores were depleted with Ca2+ -ATPase blocker, thapsigargin (TG), or histamine, 
      the capacitative Ca2+ entry (CCE) was observed. In whole cell patch clamp mode, 
      store-operated Ca2+ currents could be recorded in cells treated with histamine 
      and thapsigargin. On the other hand, voltage-operated Ca2+ channels (VOCCs) could 
      not be elicited. The application of blockers for plasma membrane Ca2+ pump 
      (PMCAs) (carboxeosin or caloxin2A1) induced a large increase of [Ca2+]i. When the 
      Na+/Ca2+ exchangers (NCXs) were blocked by Na+ free solution or KBR7943, [Ca2+]i 
      was also elevated. Using RT-PCR, mRNAs for InsP3Rs type-1, -2, and -3, PMCA-1 and 
      -4, NCX-1, -2, and -3 could be detected. From these results, we conclude that 
      Ca2+ release from ER is mediated by InsP3Rs in mES cells before differentiation 
      and Ca2+ entry through plasma membrane is mainly mediated by the store-operated 
      Ca2+ channels (SOCs). For the Ca2+ extrusion systems, both NCXs and PMCAs play 
      important roles for maintaining the low level of [Ca2+]i.
FAU - Yanagida, Eri
AU  - Yanagida E
AD  - Department of Cardiovascular Diseases, Medical Research Institute, Tokyo Medical 
      and Dental University, Yushima, Bunkyo-ku, Japan.
FAU - Shoji, Satoshi
AU  - Shoji S
FAU - Hirayama, Yoshiyuki
AU  - Hirayama Y
FAU - Yoshikawa, Fumio
AU  - Yoshikawa F
FAU - Otsu, Keishi
AU  - Otsu K
FAU - Uematsu, Hiroshi
AU  - Uematsu H
FAU - Hiraoka, Masayasu
AU  - Hiraoka M
FAU - Furuichi, Teiichi
AU  - Furuichi T
FAU - Kawano, Seiko
AU  - Kawano S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Cell Calcium
JT  - Cell calcium
JID - 8006226
RN  - 0 (Calcium Channels)
RN  - 0 (Receptors, G-Protein-Coupled)
RN  - 0 (Sodium-Calcium Exchanger)
RN  - EC 7.2.2.10 (Calcium-Transporting ATPases)
SB  - IM
MH  - Animals
MH  - Calcium Channels/metabolism
MH  - Calcium Signaling/*physiology
MH  - Calcium-Transporting ATPases/metabolism
MH  - Cell Membrane/metabolism
MH  - Endoplasmic Reticulum/metabolism
MH  - Mice
MH  - Patch-Clamp Techniques
MH  - Pluripotent Stem Cells/*physiology
MH  - Receptors, G-Protein-Coupled/metabolism
MH  - Sodium-Calcium Exchanger/metabolism
EDAT- 2004/06/15 05:00
MHDA- 2005/02/03 09:00
CRDT- 2004/06/15 05:00
PHST- 2003/09/20 00:00 [received]
PHST- 2003/12/21 00:00 [revised]
PHST- 2004/01/16 00:00 [accepted]
PHST- 2004/06/15 05:00 [pubmed]
PHST- 2005/02/03 09:00 [medline]
PHST- 2004/06/15 05:00 [entrez]
AID - S0143416004000284 [pii]
AID - 10.1016/j.ceca.2004.01.022 [doi]
PST - ppublish
SO  - Cell Calcium. 2004 Aug;36(2):135-46. doi: 10.1016/j.ceca.2004.01.022.