16,16-Dimethyl Prostaglandin E2

Prostanoid pathway activator; Inhibits 15-hydroxy PGDH

16,16-Dimethyl Prostaglandin E2

Prostanoid pathway activator; Inhibits 15-hydroxy PGDH

16,16-Dimethyl Prostaglandin E2
5 mg
635 USD
Catalog # 72372

Prostanoid pathway activator; Inhibits 15-hydroxy PGDH

Overview

16,16-dimethyl Prostaglandin E2 (16,16-dimethyl PGE2) is a competitive inhibitor of 15-hydroxy PGDH (North et al.; Ohno et al). 16,16-dimethyl PGE2 acts as an agonist on most prostaglandin E (EP) receptor subtypes (Coleman et al.; Robert et al.) with a Kd for activation of about 1 nM (Coleman et al.). 16,16-dimethyl PGE2 is supplied in methyl acetate solution at 10 mg/mL (26 mM).

MAINTENANCE AND SELF-RENEWAL
· Increased hematopoietic stem and progenitor cell (HSPC) numbers in zebrafish aorta-gonad-mesonephros (AGM) region and mouse bone marrow (North et al.).
· Mediates the effects of WNT on zebrafish HSPC self-renewal (Goessling et al.).
Alternative Names
16,16-dimethyl PGE2
Cell Type
Hematopoietic Stem and Progenitor Cells
Species
Human, Mouse, Rat, Non-Human Primate, Other
Application
Expansion
Area of Interest
Stem Cell Biology
CAS Number
39746-25-3
Chemical Formula
C₂₂H₃₆O₅
Molecular Weight
380.5 g/mol
Purity
≥ 95%
Pathway
Prostanoid
Target
15-hydroxy PGDH

Protocols and Documentation

Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.

Document Type
Product Name
Catalog #
Lot #
Language
Catalog #
72372
Lot #
All
Language
English
Document Type
Safety Data Sheet
Catalog #
72372
Lot #
All
Language
English

Applications

This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.

Resources and Publications

Educational Materials (1)

Publications (5)

Genetic interaction of PGE2 and Wnt signaling regulates developmental specification of stem cells and regeneration. Goessling W et al. Cell 2009 MAR

Abstract

Interactions between developmental signaling pathways govern the formation and function of stem cells. Prostaglandin (PG) E2 regulates vertebrate hematopoietic stem cells (HSC). Similarly, the Wnt signaling pathway controls HSC self-renewal and bone marrow repopulation. Here, we show that wnt reporter activity in zebrafish HSCs is responsive to PGE2 modulation, demonstrating a direct interaction in vivo. Inhibition of PGE2 synthesis blocked wnt-induced alterations in HSC formation. PGE2 modified the wnt signaling cascade at the level of beta-catenin degradation through cAMP/PKA-mediated stabilizing phosphorylation events. The PGE2/Wnt interaction regulated murine stem and progenitor populations in vitro in hematopoietic ES cell assays and in vivo following transplantation. The relationship between PGE2 and Wnt was also conserved during regeneration of other organ systems. Our work provides in vivo evidence that Wnt activation in stem cells requires PGE2, and suggests the PGE2/Wnt interaction is a master regulator of vertebrate regeneration and recovery.
Prostaglandin E2 regulates vertebrate haematopoietic stem cell homeostasis. North TE et al. Nature 2007 JUN

Abstract

Haematopoietic stem cell (HSC) homeostasis is tightly controlled by growth factors, signalling molecules and transcription factors. Definitive HSCs derived during embryogenesis in the aorta-gonad-mesonephros region subsequently colonize fetal and adult haematopoietic organs. To identify new modulators of HSC formation and homeostasis, a panel of biologically active compounds was screened for effects on stem cell induction in the zebrafish aorta-gonad-mesonephros region. Here, we show that chemicals that enhance prostaglandin (PG) E2 synthesis increased HSC numbers, and those that block prostaglandin synthesis decreased stem cell numbers. The cyclooxygenases responsible for PGE2 synthesis were required for HSC formation. A stable derivative of PGE2 improved kidney marrow recovery following irradiation injury in the adult zebrafish. In murine embryonic stem cell differentiation assays, PGE2 caused amplification of multipotent progenitors. Furthermore, ex vivo exposure to stabilized PGE2 enhanced spleen colony forming units at day 12 post transplant and increased the frequency of long-term repopulating HSCs present in murine bone marrow after limiting dilution competitive transplantation. The conserved role for PGE2 in the regulation of vertebrate HSC homeostasis indicates that modulation of the prostaglandin pathway may facilitate expansion of HSC number for therapeutic purposes.
International Union of Pharmacology classification of prostanoid receptors: properties, distribution, and structure of the receptors and their subtypes. Coleman RA et al. Pharmacological reviews 1994 JUN

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