PMID- 12510803
OWN - NLM
STAT- MEDLINE
DCOM- 20030407
LR  - 20161124
IS  - 0884-0431 (Print)
IS  - 0884-0431 (Linking)
VI  - 18
IP  - 1
DP  - 2003 Jan
TI  - Ca2+ signaling mediated by IP3-dependent Ca2+ releasing and store-operated Ca2+ 
      channels in rat odontoblasts.
PG  - 30-8
AB  - In the phospholipase-C (PLC) signaling system, Ca2+ is mobilized from 
      intracellular Ca2+ stores by an action of inositol 1,4,5-trisphosphate (IP3). The 
      depletion of IP3-sensitive Ca2+ stores activates a store-operated Ca2+ entry 
      (SOCE). However, no direct evidence has been obtained about these signaling 
      pathways in odontoblasts. In this study, we investigate the characteristics of 
      the SOCE and IP3-mediated Ca2+ mobilizations in rat odontoblasts using fura-2 
      microfluorometry and a nystatin-perforated patch-clamp technique. In the absence 
      of extracellular Ca2+ ([Ca2+]o), thapsigargin (TG) evoked a transient rise in 
      intracellular Ca2+ concentration ([Ca2+]i). After TG treatment to deplete the 
      store, the subsequent application of Ca2+ resulted in a rapid rise in [Ca2+]i 
      caused by SOCE. In the absence of TG treatment, no SOCE was evoked. The Ca2+ 
      influx was dependent on [Ca2+]o (KD = 1.29 mM) and was blocked by an IP3 receptor 
      inhibitor, 2-aminoethoxydiphenyl borate (2-APB), as well as La3+ in a 
      concentration-dependent manner (IC50 = 26 microM). In TG-treated cells, an 
      elevation of [Ca2+]o from 0 to 2.5 mM elicited an inwardly rectifying current at 
      hyperpolarizing potentials with a positive reversal potential. The currents were 
      selective for Ca2+ over the other divalent cations (Ca2+ > Ba2+ > Sr2+ >> Mn2+). 
      In the absence of [Ca2+]o, carbachol, bradykinin, and 2-methylthioadenosine 
      5'triphosphate activated Ca2+ release from the store; these were inhibited by 
      2-APB. These results indicate that odontoblasts possessed Ca2+ signaling pathways 
      through the activation of store-operated Ca2+ channels by the depletion of 
      intracellular Ca2+ stores and through the IP3-induced Ca2+ release activated by 
      PLC-coupled receptors.
FAU - Shibukawa, Yoshiyuki
AU  - Shibukawa Y
AD  - Department of Physiology, Tokyo Dental College, Chiba, Japan.
FAU - Suzuki, Takashi
AU  - Suzuki T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Bone Miner Res
JT  - Journal of bone and mineral research : the official journal of the American 
      Society for Bone and Mineral Research
JID - 8610640
RN  - 0 (Boron Compounds)
RN  - 0 (Calcium Channels)
RN  - 0 (Cations, Divalent)
RN  - 6I3K30563S (Lanthanum)
RN  - 85166-31-0 (Inositol 1,4,5-Trisphosphate)
RN  - E4ES684O93 (2-aminoethoxydiphenyl borate)
RN  - EC 3.1.4.- (Type C Phospholipases)
SB  - IM
MH  - Animals
MH  - Boron Compounds/pharmacology
MH  - Calcium Channels/*metabolism
MH  - *Calcium Signaling/drug effects
MH  - Cations, Divalent/metabolism
MH  - In Vitro Techniques
MH  - Inositol 1,4,5-Trisphosphate/metabolism
MH  - Kinetics
MH  - Lanthanum/pharmacology
MH  - Odontoblasts/drug effects/*metabolism
MH  - Patch-Clamp Techniques
MH  - Rats
MH  - Rats, Wistar
MH  - Type C Phospholipases/metabolism
EDAT- 2003/01/04 04:00
MHDA- 2003/04/08 05:00
CRDT- 2003/01/04 04:00
PHST- 2003/01/04 04:00 [pubmed]
PHST- 2003/04/08 05:00 [medline]
PHST- 2003/01/04 04:00 [entrez]
AID - 10.1359/jbmr.2003.18.1.30 [doi]
PST - ppublish
SO  - J Bone Miner Res. 2003 Jan;18(1):30-8. doi: 10.1359/jbmr.2003.18.1.30.