PMID- 9316620
OWN - NLM
STAT- MEDLINE
DCOM- 19971023
LR  - 20200930
IS  - 0037-9727 (Print)
IS  - 0037-9727 (Linking)
VI  - 216
IP  - 1
DP  - 1997 Oct
TI  - Characterization of Ca2+ mobilization in the human submandibular duct cell line 
      A253.
PG  - 117-24
AB  - The regulation of Ca2+ mobilization in the human submandibular duct cell line 
      A253 was investigated by monitoring cytosolic free Ca2+ concentrations ([Ca2+]i) 
      using the Ca(2+)-sensitive fluorescent indicator fura-2 and by measuring inositol 
      1,4,5-triphosphate (IP3) formation. An increase in [Ca2+]i was elicited by ATP, 
      isoproterenol (IPR), or vasoactive intestinal polypeptide (VIP), but not by 
      acetylcholine, norepinephrine, or substance P, suggesting that Ca2+ mobilization 
      is regulated by P2-purinergic, beta 2-adrenergic, and VIP receptors. 1,4,5-IP3 
      formation was significantly increased by ATP but not by the other agonists. 
      Exposure of the cells to a membrane permeable cAMP analog, dibutyryl-cAMP, or to 
      the adenylate cyclase activator forskolin induced a smaller increase in [Ca2+]i, 
      indicating that the IPR-induced Ca2+ release is not mediated by cyclic AMP. 
      Inhibition of the endoplasmic Ca(2+)-ATPase with thapsigargin (TG) in Ca(2+)-free 
      medium induced a 207% increase in [Ca2+]i, and a subsequent exposure to ATP 
      caused a further increase in [Ca2+]i of 104%. Similarly, TG exposure after ATP 
      induced a further Ca2+ release, suggesting that the TG-sensitive store and the 
      IP3-sensitive store do not overlap. Similar results were observed by sequential 
      exposure to TG and IPR or to ATP and IPR. Ca2+ influx across the plasma membrane 
      was enhanced after ATP or TG, but not after IPR. Our findings show a unique 
      pattern of Ca2+ mobilization in the A253 cell line: (i) Ca2+ mobilization is 
      regulated by P2-purinergic, beta 2-adrenergic, and VIP receptors; (ii) Ca2+ 
      release is mediated by 1,4,5-IP3 and probably by an unknown mediator; (iii) TG, 
      P2-, and beta 2-agonists discharge separate Ca2+ stores; and (iv) ATP and TG, but 
      not IPR, regulate Ca2+ influx.
FAU - Zhang, G H
AU  - Zhang GH
AD  - Department of Pediatrics, University of Texas Health Science Center at San 
      Antonio 78284, USA.
FAU - Helmke, R J
AU  - Helmke RJ
FAU - Martinez, J R
AU  - Martinez JR
LA  - eng
GR  - DE09270/DE/NIDCR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Proc Soc Exp Biol Med
JT  - Proceedings of the Society for Experimental Biology and Medicine. Society for 
      Experimental Biology and Medicine (New York, N.Y.)
JID - 7505892
RN  - 63X7MBT2LQ (Bucladesine)
RN  - 67526-95-8 (Thapsigargin)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - L628TT009W (Isoproterenol)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Adenosine Triphosphate/pharmacology
MH  - Bucladesine/pharmacology
MH  - Calcium/*metabolism
MH  - Cell Line
MH  - Humans
MH  - Isoproterenol/pharmacology
MH  - Submandibular Gland/*metabolism
MH  - Thapsigargin/pharmacology
EDAT- 1997/10/08 00:00
MHDA- 1997/10/08 00:01
CRDT- 1997/10/08 00:00
PHST- 1997/10/08 00:00 [pubmed]
PHST- 1997/10/08 00:01 [medline]
PHST- 1997/10/08 00:00 [entrez]
AID - 10.3181/00379727-216-44162c [doi]
PST - ppublish
SO  - Proc Soc Exp Biol Med. 1997 Oct;216(1):117-24. doi: 10.3181/00379727-216-44162c.