Prostaglandin E2 (PGE2) is a naturally occurring hormone involved in a variety of physiological processes in the body, including smooth muscle contraction and relaxation, regulation of vasodilatation and constriction, regulation of blood pressure, and inflammatory regulation.

METHODS: Human colorectal cancer cells LS-174T were treated with Prostaglandin E2 (0.05-10 μM) for 1-60 min, and the expression levels of target proteins were detected by Western Blot.
RESULTS: Prostaglandin E2 induced phosphorylation of Akt as early as 1 min after stimulation, and the activation of Akt reached a maximum within 10 min and persisted until 60 min. The addition of Prostaglandin E2 activated Akt in a dose-dependent manner. [1]
METHODS: FDC-like cells were treated with Prostaglandin E2 (1 μM) for 15-120 min, and the expression levels of target proteins were detected by Western Blot.
RESULTS: Prostaglandin E2 did not increase p-ERK, but decreased p-ERK at 60 and 120 min. on the contrary, p-p38 increased starting at 15 min and continued to 60 min. [2]

METHODS: To test the role of EP2 receptors in the in vivo absorption response, Prostaglandin E2 (3 mg/kg) was injected subcutaneously four times daily for three days into EP2+/+ and EP2-/- mice on a 129/SvEv background.
RESULTS: Prostaglandin E2 increased serum calcium from 9.8+/-0.5 to 10.7+/-0.3 mg/dL in EP2+/+ mice but not in EP2-/- mice. [3]
METHODS: To study the effects on bone, Prostaglandin E2 (6 mg/kg) was injected subcutaneously into C57BL/6 mice once daily for 3-12 days.
RESULTS: Prostaglandin E2-treated mice showed a decrease in trabecular bone volume (BV/TV) at 14 days, indicating increased bone resorption. However, the Prostaglandin E2-treated 3-day group also stimulated bone formation at 14 days due to increased mineral deposition rate (MAR) and bone formation rate (BFR/BS). [4]