PMID- 11684033
OWN - NLM
STAT- MEDLINE
DCOM- 20020123
LR  - 20190717
IS  - 0003-9969 (Print)
IS  - 0003-9969 (Linking)
VI  - 46
IP  - 12
DP  - 2001 Dec
TI  - Regulation of Ca(2+) signals in a parotid cell line Par-C5.
PG  - 1141-9
AB  - The Ca(2+) signaling system in an established immortalized rat parotid acinar 
      cell line, Par-C5, was examined using the Ca(2+)-sensitive fluorescent indicator 
      fura-2 and by measuring inositol 1,4,5-trisphosphate (IP(3)) formation. 
      Agonist-induced increase in intracellular Ca(2+) ([Ca(2+)](i)) by mobilization of 
      intracellular stores and influx across the cell membrane was stimulated by 
      acetylcholine (ACh) and ATP, whereas noradrenaline-(NA)-induced a small 
      [Ca(2+)](i) increase mediated primarily by release from intracellular Ca(2+) 
      stores. [Ca(2+)](i) increase by ACh and ATP was mediated through the 
      phosphoinositide signal pathway since both agonists significantly increased 
      1,4,5-IP(3) formation and Ca(2+) mobilization was abolished by the phospholipase 
      C inhibitor U73122. In Ca(2+)-free medium, ACh or ATP discharged the 
      IP(3)-sensitive Ca(2+) store and essentially abolished subsequent [Ca(2+)](i) 
      response to thapsigargin (TG). Exposure to ionomycin and monensin after TG 
      induced a further mobilization of Ca(2+), suggesting IP(3)-insensitive stores are 
      present. Furthermore, depletion of IP(3)-sensitive Ca(2+) stores by TG, ACh and 
      ATP enhanced plasmalemmal Ca(2+)-entry pathways. Exposure to tumor necrosis 
      factor-alpha (TNF-alpha), a cytokine associated with lymphocyte invasion of 
      salivary epithelial cells in autoimmune disorders, significantly reduced 
      ACh-stimulated Ca(2+) mobilization. TNF-alpha inhibitory effect on Ca(2+) 
      mobilization was not directly due to an interaction on muscarinic receptors since 
      ACh-induced 1,4,5-IP(3) formation was not altered. These results in the Par-C5 
      cell line indicate 1) [Ca(2+)](i) is regulated by muscarinic and P2Y-nucleotide 
      receptors and partly by alpha(1)-adrenergic receptors; 2) IP(3)-sensitive and 
      -insensitive Ca(2+) stores exist; 3) Ca(2+) influx activated by ACh, ATP or TG is 
      mediated by the store-operated Ca(2+) entry pathway; and 4) muscarinic 
      agonist-stimulated Ca(2+) mobilization is altered by the cytokine TNF-alpha.
FAU - Liu, X
AU  - Liu X
AD  - Secretory Cell Physiology Laboratory, Department of Pediatrics, University of 
      Texas Health Center, Mail Code 7827, 7703 Floyd Curl Dr., San Antonio, TX 
      78229-3900, USA.
FAU - Mork, A C
AU  - Mork AC
FAU - Sun, X
AU  - Sun X
FAU - Castro, R
AU  - Castro R
FAU - Martinez, J R
AU  - Martinez JR
FAU - Zhang, G H
AU  - Zhang GH
LA  - eng
GR  - DE09270/DE/NIDCR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Arch Oral Biol
JT  - Archives of oral biology
JID - 0116711
RN  - 0 (Adrenergic alpha-Agonists)
RN  - 0 (Calcium Channel Agonists)
RN  - 0 (Muscarinic Agonists)
RN  - 0 (P2ry2 protein, rat)
RN  - 0 (Purinergic P2 Receptor Agonists)
RN  - 0 (Receptors, Adrenergic, alpha)
RN  - 0 (Receptors, Muscarinic)
RN  - 0 (Receptors, Purinergic P2)
RN  - 0 (Receptors, Purinergic P2Y2)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 85166-31-0 (Inositol 1,4,5-Trisphosphate)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Adrenergic alpha-Agonists/pharmacology
MH  - Analysis of Variance
MH  - Animals
MH  - Calcium/agonists/*metabolism
MH  - Calcium Channel Agonists/metabolism
MH  - Calcium Signaling/drug effects/*physiology
MH  - Cell Line, Transformed
MH  - Inositol 1,4,5-Trisphosphate/biosynthesis
MH  - Muscarinic Agonists/pharmacology
MH  - Parotid Gland/cytology/*metabolism
MH  - Purinergic P2 Receptor Agonists
MH  - Rats
MH  - Receptors, Adrenergic, alpha/physiology
MH  - Receptors, Muscarinic/physiology
MH  - Receptors, Purinergic P2/physiology
MH  - Receptors, Purinergic P2Y2
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 2001/10/31 10:00
MHDA- 2002/01/24 10:01
CRDT- 2001/10/31 10:00
PHST- 2001/10/31 10:00 [pubmed]
PHST- 2002/01/24 10:01 [medline]
PHST- 2001/10/31 10:00 [entrez]
AID - S0003996901000747 [pii]
AID - 10.1016/s0003-9969(01)00074-7 [doi]
PST - ppublish
SO  - Arch Oral Biol. 2001 Dec;46(12):1141-9. doi: 10.1016/s0003-9969(01)00074-7.