PMID- 16512814
OWN - NLM
STAT- MEDLINE
DCOM- 20060823
LR  - 20181201
IS  - 0105-4538 (Print)
IS  - 0105-4538 (Linking)
VI  - 61
IP  - 4
DP  - 2006 Apr
TI  - Prostaglandin E potentiates the immunologically stimulated histamine release from 
      human peripheral blood-derived mast cells through EP1/EP3 receptors.
PG  - 503-6
AB  - BACKGROUND: Mast cells cultured from human peripheral blood have been widely used 
      to study human mast cell function. Prostanoids are the important regulators of 
      mast cell activity, however, there were no reports about the class of prostanoid 
      receptors expressed on such cultured cells. AIMS: The present study was to 
      characterize pharmacologically the prostanoid receptors by investigating the 
      effects of prostanoid receptor agonists on the immunoglobulin E (IgE)-mediated 
      histamine release from the cultured mast cells. METHODS: Mast cells cultured from 
      human progenitor cells in peripheral blood were sensitized with human myeloma 
      IgE, and then challenged with anti-human IgE following pretreatment with diverse 
      prostanoid receptor agonists. The histamine content in supernatants and cell 
      pellets were measured by histamine auto-analyzer. RESULTS: Of the prostanoid 
      receptor agonists tested, the prostaglandin E2 (PGE2) receptor (EP receptor) 
      agonist PGE2 (10(-7) to 10(-11) M) produced concentration-related potentiation of 
      IgE-mediated histamine release from the cultured mast cells. Sulprostone, an 
      EP1/EP3 agonist, SC-46275, a selective EP3 agonist, and 11-deoxy-PGE1, a 
      selective EP2/EP3/EP4 agonist also caused a significant increase in histamine 
      release induced by anti-IgE. BW245C, fluprostone, cicaprost and U46619 for the 
      prostaglandin D2, F2alpha, I2, and thromboxane A2 receptors respectively, and the 
      EP2/EP4 receptor agonist butaprost had little effect on anti-IgE stimulated 
      histamine release from mast cells. CONCLUSIONS: The present results suggest that 
      PGE2 potentiates the IgE-mediated histamine release from the cultured mast cell 
      via EP3 and/or EP1 receptors.
FAU - Wang, X S
AU  - Wang XS
AD  - Department of Pharmacology, Faculty of Medicine, Chinese University of Hong Kong, 
      New Territories, Hong Kong, China.
FAU - Lau, H Y A
AU  - Lau HY
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Denmark
TA  - Allergy
JT  - Allergy
JID - 7804028
RN  - 0 (PTGER1 protein, human)
RN  - 0 (PTGER3 protein, human)
RN  - 0 (Receptors, Prostaglandin E)
RN  - 0 (Receptors, Prostaglandin E, EP1 Subtype)
RN  - 0 (Receptors, Prostaglandin E, EP3 Subtype)
RN  - 137255-19-7 (SC-46275)
RN  - F5TD010360 (Alprostadil)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Alprostadil/analogs & derivatives/pharmacology
MH  - Blood Cells/cytology
MH  - Cells, Cultured
MH  - Dinoprostone/*pharmacology
MH  - Dose-Response Relationship, Drug
MH  - Histamine Release/*drug effects
MH  - Humans
MH  - Mast Cells/*drug effects/metabolism
MH  - Receptors, Prostaglandin E/*physiology
MH  - Receptors, Prostaglandin E, EP1 Subtype
MH  - Receptors, Prostaglandin E, EP3 Subtype
EDAT- 2006/03/04 09:00
MHDA- 2006/08/24 09:00
CRDT- 2006/03/04 09:00
PHST- 2006/03/04 09:00 [pubmed]
PHST- 2006/08/24 09:00 [medline]
PHST- 2006/03/04 09:00 [entrez]
AID - ALL1043 [pii]
AID - 10.1111/j.1398-9995.2006.01043.x [doi]
PST - ppublish
SO  - Allergy. 2006 Apr;61(4):503-6. doi: 10.1111/j.1398-9995.2006.01043.x.