There is an increasing body of evidence that prostanoids modulate mast cell functions and contribute to the development of allergic inflammation. The present study aimed to identify an undetermined function of prostaglandin (PG) F2α in mast cell activation and the signaling mechanism involved in it. Simultaneous quantification of prostanoids by liquid chromatography/tandem mass spectrometry revealed the constitutive release of PGF2α, thromboxane B2, and 6-keto-PGF1α from bone marrow-derived mast cells (BMMCs). Upon activation of BMMCs by lipopolysaccharide, the cytokine production in BMMCs was enhanced when the culture was supplemented with PGF2α. However, F prostanoid receptor-a selective receptor for PGF2α-was not detected in BMMCs. Further investigations performed using prostanoid receptor antagonists revealed an alternative mechanism wherein the receptors for PGE species-E prostanoid receptors-mediated the PGF2α signal in BMMCs. The present study provides an insight into a novel function of PGF2α, i.e., an autocrine accelerator for mast cell activation.
|ジャーナル||Biochemical and biophysical research communications|
|出版ステータス||Published - 2008 3 14|
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology