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PGE2; Dinoprostone; 9-Oxo-11α,15S-dihydroxy-prosta-5Z,13E-dien-1-oic acid; Prostin E2; Prepidil; NSC165560; 11α,15α-Dihydroxy-9-oxo-5-cis,13-trans-prostadienoic acid

Chemical

C20H32O5

352.5

14: 7877

363-24-6

UK8000000

Synthetic (originally isolated from sheep prostate).

≥98%

White solid.

Soluble in ethanol (50 mg/ml), DMSO (50 mg/ml) or DMF (100 mg/ml). Sparingly soluble in PBS, pH 7.2 (5mg/ml).

Multi-species

Do not add PGE2 to basic solution with pH>7.4.

XEYBRNLFEZDVAW-ARSRFYASSA-N

BLUE ICE

+4°C

-20°C

Keep cool and dry.Protect from light.

Stable for at least 2 years after receipt when stored at -20°C.

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• One of the most typical lipid mediators produced from arachidonic acid (AA) by cyclooxygenase (COX) as the rate-limiting enzyme and acts on four kinds of receptor subtypes (EP1, EP2, EP3 and EP4) with high binding affinity (Kd values range between ~1-10nM).
• Regulator of numerous physiological functions ranging from reproduction to neuronal, metabolic and immune functions.
• Implied in the regulation of body temperature and sleep-wake activity. Regulating factor for bone formation and bone healing. Potent vasodilator. Influences smooth muscle relaxation, fertility and gastric mucosal integrity (first line of defense of the intestinal immune system).
• Acts as a pro-inflammatory mediator, but also exerts anti-inflammatory responses. As pro-inflammatory mediator, PGE2 contributes to the regulation of the cytokine expression profile of DCs and has been reported to bias T cell differentiation towards a T helper (Th) 1 or Th2 response. Exerts anti-inflammatory actions on innate immune cells like neutrophils, monocytes and NK cells.
• Implicated in various tumorigenic processes. Facilitates tumor progression through stimulation of angiogenesis via EP2, mediates cell invasion and metastasis formation via EP4 and promotes cell survival by inhibiting apoptosis via numerous signaling pathways. Tumor cell-produced PGE2 has been implicated in strategies of tumors for evasion of immune surveillance. Furthermore, it can enhance the inhibitory function of human regulatory T cells.
• Regulates vertebrate hematopoietic stem cell (HSC) homeostasis.
• Inhibits NLRP3 by acting through receptor EP4 activation that increases cAMP. cAMP activates PKA that phosphorylates NLRP3 at serine 295. PKA phosphorylation of NLRP3 inhibits the NLRP3 ATPase activity, which is required for assembly of NLRP3-ASC complexes.

Product References

Prostaglandin E2 at new glance: novel insights in functional diversity offer therapeutic chances: D. F. Legler, et al.; Int. J. Biochem. Cell Biol. 42, 198 (2010) (Review)

Prostaglandin E2, an immunoactivator: D. Sakata, et al.; J. Pharmacol. Sci. 112, 1 (2010) (Review)

Newly emerging roles for prostaglandin E2 regulation of hematopoiesis and hematopoietic stem cell engraftment: E.M. Durand, et al.; Curr. Opin. Hematol. 17, 308 (2010) (Review)

Prostanoid signaling: dual role for prostaglandin E2 in neurotoxicity: D. Milatovic, et al.; Neurotoxicol. 32, 312 (2011) (Review)

Prostaglandin E2 EP receptors as therapeutic targets in breast cancer: J. Reader, et al.; Cancer Metastasis Rev. 30, 449 (2011) (Review)

Prostaglandin E2 and T cells: friends or foes? V. Sreeramkumar, et al.; Immunol. Cell Biol. 90, 579 (2012) (Review)

Regulation of immune responses by prostaglandin E2: P. Kalinski; J. Immunol. 188, 21 (2012) (Review)

Polarization of the innate immune response by prostaglandin E2: a puzzle of receptors and signals: M. Rodriguez, et al.; Mol. Pharmacol. 85, 187 (2014) (Review)

Prostaglandin E2-induced inflammation: Relevance of prostaglandin E receptors: K. Kawahara, et al.; Biochim. Biophys Acta. 1851, 414 (2015) (Review)

Prostaglandin E2 and the EP receptors in malignancy: possible therapeutic targets? G. OCallaghan & A. Houston; Br. J. Pharmacol. 172, 5239 (2015) (Review)

Prostaglandin E2 Inhibits NLRP3 Inflammasome Activation through EP4 Receptor and Intracellular Cyclic AMP in Human Macrophages: M. Sokolowska, et al.; J. Immunol. 194, 5472 (2015)

NLRP3 inflammasome inhibition is disrupted in a group of auto-inflammatory disease CAPS mutations: L. Mortimer, et al.; Nat. Immunol. (Epub ahead of print) (2016)

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