PMID- 1304434
OWN - NLM
STAT- MEDLINE
DCOM- 19930702
LR  - 20181130
IS  - 0252-1164 (Print)
IS  - 0252-1164 (Linking)
VI  - 9
IP  - 2
DP  - 1992
TI  - Activation of PGE2-secretion from gastric mucosa by a type I phospholipase C is 
      mediated by a direct release of arachidonic acid.
PG  - 78-86
AB  - We investigated the effects of an exogenous Type I phospholipase C (PLC) from 
      clostridium perfringens on arachidonic acid release and prostaglandin synthesis 
      from gastric mucosa by determining PGE2 release from organ cultured rabbit 
      mucosal biopsies as well as PGE2 synthesis and substrate-dependent inactivation 
      of the prostaglandin cyclooxygenase from endogenously released arachidonic acid 
      in mucosal homogenate. PLC dose dependently stimulated PGE2 secretion from organ 
      cultured mucosa to 145% and 245% at 0.1 and 1.0 U/ml during a 60 minute culture 
      period. This effect was not affected by the calmodulin antagonist 
      N-(6-aminohexyl)-1-5-chloro-1-naphthalene-sulfonamide (W-7) or the intracellular 
      calcium chelator 1,2-bis-(2-aminophenoxy)ethane-N,N,N',N',-tetraacetic 
      acid-acetoxymethyl ester (BAPTA-AM). PLC could not be substituted by 
      phorbol-12-myristate 13-acetate (PMA), an analogue of the diacylglycerol second 
      messenger functions. During a 15 minute preincubation of mucosal homogenate at 37 
      degrees C, 1mM CaCl2 stimulated PGE2 synthesis from endogenous arachidonic acid 
      about 5-fold compared to an EDTA-control. In contrast, the residual prostaglandin 
      synthesizing capacity, determined by incubation with excess 14C-labelled 
      arachidonic acid, was reduced by CaCl2 to 37% of the EDTA-value. Quinacrine, an 
      inhibitor of arachidonic acid release from phosphatidylethanolamine, reduced both 
      the stimulation of PGE2 synthesis and the inactivation of prostaglandin 
      cyclooxygenase. Therefore we conclude, that this Ca(2+)-effect reflects 
      activation of the Ca-dependent phospholipase A2 (PLA2) and, as a consequence, 
      substrate-induced inactivation of the prostaglandin cyclooxygenase.(ABSTRACT 
      TRUNCATED AT 250 WORDS)
FAU - Preclik, G
AU  - Preclik G
AD  - University of Ulm, Department of Internal Medicine II, Germany.
FAU - Stange, E F
AU  - Stange EF
FAU - Ditschuneit, H
AU  - Ditschuneit H
LA  - eng
PT  - Journal Article
PL  - Germany
TA  - Clin Physiol Biochem
JT  - Clinical physiology and biochemistry
JID - 8305885
RN  - 0 (Calmodulin)
RN  - 0 (Sulfonamides)
RN  - 139890-68-9 (1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid 
      acetoxymethyl ester)
RN  - 27YG812J1I (Arachidonic Acid)
RN  - 526U7A2651 (Egtazic Acid)
RN  - 65595-90-6 (W 7)
RN  - EC 3.1.- (Phospholipases)
RN  - EC 3.1.4.- (Type C Phospholipases)
RN  - K7Q1JQR04M (Dinoprostone)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Arachidonic Acid/*metabolism
MH  - Calcium/pharmacology
MH  - Calmodulin/antagonists & inhibitors
MH  - Dinoprostone/biosynthesis/*metabolism
MH  - Dose-Response Relationship, Drug
MH  - Egtazic Acid/analogs & derivatives/pharmacology
MH  - Gastric Mucosa/drug effects/*metabolism
MH  - Male
MH  - Organ Culture Techniques
MH  - Phospholipases/antagonists & inhibitors
MH  - Rabbits
MH  - Radioimmunoassay
MH  - Sulfonamides/pharmacology
MH  - Type C Phospholipases/*metabolism
EDAT- 1992/01/01 00:00
MHDA- 1992/01/01 00:01
CRDT- 1992/01/01 00:00
PHST- 1992/01/01 00:00 [pubmed]
PHST- 1992/01/01 00:01 [medline]
PHST- 1992/01/01 00:00 [entrez]
PST - ppublish
SO  - Clin Physiol Biochem. 1992;9(2):78-86.