Phosphatidyl inositide 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) pathways are modulated by prostaglandin E₂ in mannitol-stimulated mast cells.

<p>Cells were treated in Tyrode’s buffer for 15 minutes with either 10% mannitol stimulation and/or PGE₂ at 10 µM. EP receptor antagonist pretreatment was done 10 minutes before any cell stimulation as follows: AH6809 (10 µM) blocking receptors EP₁ and EP₂, L826266 (30 µM) blocking receptor EP₃, and AH23848 (10 µM) blocking receptor EP₄. Western Blot analysis was performed in LAD2 cells (A) and HMC-1 (B) to explore (1) AKT phosphorylation as a surrogate marker for PI3K activation, and (2) MAPK activation via JNK, ERK1/2, and p38 phosphorylation. Blot against β-actin was performed (as a loading control). The data is representative of three independent experiments.