PMID- 10025666
OWN - NLM
STAT- MEDLINE
DCOM- 19990429
LR  - 20191024
IS  - 0730-2312 (Print)
IS  - 0730-2312 (Linking)
VI  - 72
IP  - 1
DP  - 1999 Jan 1
TI  - Modulation of Ca2+ mobilization by protein kinase C in rat submandibular acinar 
      cells.
PG  - 47-55
AB  - The effects of protein kinase C (PKC) activation and inhibition on the inositol 
      1,4,5-trisphosphate (IP3) and cytosolic Ca2+ ([Ca2+]i) responses of rat 
      submandibular acinar cells were investigated. IP3 formation in response to 
      acetylcholine (ACh) was not affected by the PKC activator phorbol 12-myristate 
      13-acetate (PMA), nor by the PKC inhibitor calphostin C (CaC). The ACh-elicited 
      initial increase in [Ca2+]i in the absence of extracellular Ca2+ was not changed 
      by short-term (0.5 min) exposure to PMA, but significantly reduced by long-term 
      (30 min) exposure to PMA, and also by pre-exposure to the PKC inhibitors CaC and 
      chelerythrine chloride (ChC). After ACh stimulation, subsequent exposure to 
      ionomycin caused a significantly (258%) larger [Ca2+]i increase in CaC-treated 
      cells than in control cells. However, pre-exposure to CaC for 30 min did not 
      alter the Ca2+ release induced by ionomycin alone. These results suggest that the 
      reduction of the initial [Ca2+]i increase is due to an inhibition of the Ca2+ 
      release mechanism and not to store shrinkage. The thapsigargin (TG)-induced 
      increase in [Ca2+]i was significantly reduced by short-term (0.5 min), but not by 
      long-term (30 min) exposure to PMA, nor by pre-exposure to ChC or CaC. Subsequent 
      exposure to ionomycin after TG resulted in a significantly (70%) larger [Ca2+]i 
      increase in PMA-treated cells than in control cells, suggesting that activation 
      of PKC slows down the Ca2+ efflux or passive leak seen in the presence of TG. 
      Taken together, these results indicate that inhibition of PKC reduces the 
      IP3-induced Ca2+ release and activation of PKC reduces the Ca2+ efflux seen after 
      inhibition of the endoplasmic Ca2+-ATPase in submandibular acinar cells.
FAU - Mork, A C
AU  - Mork AC
AD  - Department of Pediatrics, University of Texas Health Science Center at San 
      Antonio, 78284, USA.
FAU - Zhang, G H
AU  - Zhang GH
FAU - Martinez, J R
AU  - Martinez JR
LA  - eng
GR  - DE09270/DE/NIDCR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Cell Biochem
JT  - Journal of cellular biochemistry
JID - 8205768
RN  - 0 (Alkaloids)
RN  - 0 (Benzophenanthridines)
RN  - 0 (Naphthalenes)
RN  - 0 (Phenanthridines)
RN  - 0 (Phorbol Esters)
RN  - 0 (calphostin complex)
RN  - 56092-81-0 (Ionomycin)
RN  - 67526-95-8 (Thapsigargin)
RN  - 85166-31-0 (Inositol 1,4,5-Trisphosphate)
RN  - E3B045W6X0 (chelerythrine)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - N9YNS0M02X (Acetylcholine)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Acetylcholine/pharmacology
MH  - Alkaloids
MH  - Animals
MH  - Benzophenanthridines
MH  - Calcium/*metabolism
MH  - Cells, Cultured
MH  - Enzyme Activation/drug effects
MH  - Inositol 1,4,5-Trisphosphate/metabolism
MH  - Ionomycin/pharmacology
MH  - Male
MH  - Naphthalenes/pharmacology
MH  - Phenanthridines/pharmacology
MH  - Phorbol Esters/pharmacology
MH  - Protein Kinase C/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Signal Transduction/physiology
MH  - Submandibular Gland/enzymology/*metabolism
MH  - Thapsigargin/pharmacology
EDAT- 1999/02/20 03:12
MHDA- 2000/06/20 09:00
CRDT- 1999/02/20 03:12
PHST- 1999/02/20 03:12 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1999/02/20 03:12 [entrez]
AID - 10.1002/(SICI)1097-4644(19990101)72:1<47::AID-JCB6>3.0.CO;2-I [pii]
AID - 10.1002/(sici)1097-4644(19990101)72:1<47::aid-jcb6>3.3.co;2-9 [doi]
PST - ppublish
SO  - J Cell Biochem. 1999 Jan 1;72(1):47-55. doi: 
      10.1002/(sici)1097-4644(19990101)72:1<47::aid-jcb6>3.3.co;2-9.