PMID- 11483409
OWN - NLM
STAT- MEDLINE
DCOM- 20010927
LR  - 20190921
IS  - 0898-6568 (Print)
IS  - 0898-6568 (Linking)
VI  - 13
IP  - 8
DP  - 2001 Aug
TI  - Mechanisms of bradykinin-mediated Ca(2+) signalling in canine cultured corneal 
      epithelial cells.
PG  - 565-74
AB  - Experiments were designed to differentiate the mechanisms of bradykinin receptors 
      mediating the changes in intracellular Ca(2+) concentration ([Ca(2+)](i)) in 
      canine cultured corneal epithelial cells (CECs). Bradykinin and Lys-bradykinin 
      caused an initial transient peak of [Ca(2+)](i) in a concentration-dependent 
      manner, with half-maximal stimulation (pEC(50)) obtained at 6.9 and 7.1, 
      respectively. Pretreatment of CECs with pertussis toxin (PTX) or cholera toxin 
      (CTX) for 24 h did not affect the bradykinin-induced [Ca(2+)](i) changes. 
      Application of Ca(2+) channel blockers, diltiazem and Ni(2+), inhibited the 
      bradykinin-induced Ca(2+) mobilization, indicating that Ca(2+) influx was 
      required for the bradykinin-induced responses. Addition of thapsigargin (TG), 
      which is known to deplete intracellular Ca(2+) stores, transiently increased 
      [Ca(2+)](i) in Ca(2+)-free buffer, and subsequently induced Ca(2+) influx when 
      Ca(2+) was readded to this buffer. Pretreatment of CECs with TG completely 
      abolished bradykinin-induced initial transient [Ca(2+)](i), but had slight effect 
      on bradykinin-induced Ca(2+) influx. Pretreatment of CECs with 
      1-[beta-[3-(4-methoxyphenyl)propoxy]-4-methoxyphenethyl]-1H-imidazole (SKF96365) 
      and 
      1-(6-((17beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione 
      (U73122) inhibited the bradykinin-induced Ca(2+) release and Ca(2+) influx, 
      consistent with the inhibition of receptor-gated Ca(2+) channels and 
      phospholipase C (PLC) in CECs, respectively. These results demonstrate that 
      bradykinin directly stimulates B(2) receptors and subsequently Ca(2+) 
      mobilization via a PTX-insensitive G protein in canine CECs. These results 
      suggest that bradykinin-induced Ca(2+) influx into the cells is not due to 
      depletion of these Ca(2+) stores, as prior depletion of these pools by TG has no 
      effect on the bradykinin-induced Ca(2+) influx that is dependent on extracellular 
      Ca(2+) in CECs.
FAU - Huang, S C
AU  - Huang SC
AD  - Department of Ophthalmology, College of Medicine, Chang Gung University, 
      Kwei-San, Tao-Yuan, Taiwan, ROC.
FAU - Chien, C
AU  - Chien C
FAU - Hsiao, L
AU  - Hsiao L
FAU - Wang, C
AU  - Wang C
FAU - Chiu, C
AU  - Chiu C
FAU - Liang, K
AU  - Liang K
FAU - Yang, C
AU  - Yang C
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Cell Signal
JT  - Cellular signalling
JID - 8904683
RN  - 0 (Calcium Channel Blockers)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Estrenes)
RN  - 0 (Imidazoles)
RN  - 0 (Pyrrolidinones)
RN  - 0 (Virulence Factors, Bordetella)
RN  - 112648-68-7 
      (1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione)
RN  - 67526-95-8 (Thapsigargin)
RN  - 9012-63-9 (Cholera Toxin)
RN  - EC 2.4.2.31 (Pertussis Toxin)
RN  - EC 3.1.4.- (Type C Phospholipases)
RN  - I61V87164A (1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole)
RN  - S8TIM42R2W (Bradykinin)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Bradykinin/*pharmacology
MH  - Calcium/metabolism
MH  - Calcium Channel Blockers/pharmacology
MH  - *Calcium Signaling
MH  - Cells, Cultured
MH  - Cholera Toxin/pharmacology
MH  - Dogs
MH  - Enzyme Inhibitors/pharmacology
MH  - Epithelium, Corneal/*metabolism
MH  - Estrenes/pharmacology
MH  - Imidazoles/pharmacology
MH  - Pertussis Toxin
MH  - Pyrrolidinones/pharmacology
MH  - Thapsigargin/pharmacology
MH  - Type C Phospholipases/antagonists & inhibitors
MH  - Virulence Factors, Bordetella/pharmacology
EDAT- 2001/08/03 10:00
MHDA- 2001/09/28 10:01
CRDT- 2001/08/03 10:00
PHST- 2001/08/03 10:00 [pubmed]
PHST- 2001/09/28 10:01 [medline]
PHST- 2001/08/03 10:00 [entrez]
AID - S089865680100170X [pii]
AID - 10.1016/s0898-6568(01)00170-x [doi]
PST - ppublish
SO  - Cell Signal. 2001 Aug;13(8):565-74. doi: 10.1016/s0898-6568(01)00170-x.