View source for Biology:Prostaglandin E2 receptor

{{Short description|G protein-coupled receptor}}
{{DISPLAYTITLE:Prostaglandin E<sub>2</sub> receptor}}
The '''prostaglandin E<sub>2</sub>''' ('''PGE<sub>2</sub>''') '''receptors''' are [[Biology:G protein-coupled receptor|G protein-coupled receptor]]s that bind and are activated by [[Chemistry:Prostaglandin E2|prostaglandin E<sub>2</sub>]]. They are members of the prostaglandin receptors class of [[Biology:Receptor (biochemistry)|receptors]] and include the following [[Biology:Protein isoform|Protein isoform]]s:

* [[Biology:Prostaglandin EP1 receptor|Prostaglandin E<sub>2</sub> receptor 1]] (EP<sub>1</sub>) - {{Gene|PTGER1}}
* [[Biology:Prostaglandin EP2 receptor|Prostaglandin E<sub>2</sub> receptor 2]] (EP<sub>2</sub>) - {{Gene|PTGER2}}
* [[Biology:Prostaglandin EP3 receptor|Prostaglandin E<sub>2</sub> receptor 3]] (EP<sub>3</sub>) - {{Gene|PTGER3}}
* [[Biology:Prostaglandin EP4 receptor|Prostaglandin E<sub>2</sub> receptor 4]] (EP<sub>4</sub>) - {{Gene|PTGER4}}

==Studies==
An antagonist of a prostaglandin E2 receptor has been shown to serve as an affective contraceptive for female [[Biology:Macaque|macaques]] while unaffecting their menstrual cyclicity as well as hormonal patterns. The exact reason behind the reduced amount of successful pregnancies of primates during the study is unclear due a number of possibilities that may affect such result.<ref>{{cite journal |last1=Peluffo |first1=M.C. |last2=Stanley |first2=J. |last3=Braeuer |first3=N. |last4=Rotgeri |first4=A. |last5=Fritzemeier |first5=K.-H. |last6=Fuhrmann |first6=U. |last7=Buchmann |first7=B. |last8=Adevai |first8=T. |last9=Murphy |first9=M.J. |last10=Zelinski |first10=M.B. |last11=Lindenthal |first11=B. |last12=Hennebold |first12=J.D. |last13=Stouffer |first13=R.L. |title=A prostaglandin E2 receptor antagonist prevents pregnancies during a preclinical contraceptive trial with female macaques |journal=Human Reproduction |date=July 2014 |volume=29 |issue=7 |pages=1400–1412 |doi=10.1093/humrep/deu083|pmid=24781425 |pmc=4059334 }}</ref>
Inhibition of the prostaglandin E2 EP<sub>4</sub> receptor has been shown to inhibit tumor growth, [[Biology:Angiogenesis|angiogenesis]], lymphangiogenesis, and [[Medicine:Metastasis|metastasis]]. <ref>{{cite journal |last1=Majumder |first1=Mousumi |last2=Xin |first2=Xiping |last3=Liu |first3=Ling |last4=Girish |first4=Gannareddy V. |last5=Lala |first5=Peeyush K. |title=Prostaglandin E2 receptor EP4 as the common target on cancer cells and macrophages to abolish angiogenesis, lymphangiogenesis, metastasis, and stem-like cell functions |journal=Cancer Science |date=September 2014 |volume=105 |issue=9 |pages=1142–1151 |doi=10.1111/cas.12475|pmid=24981602 |pmc=4462388 }}</ref><ref>{{cite journal |last1=Han |first1=ShouWei |last2=Roman |first2=Jesse |title=Suppression of prostaglandin E2 receptor subtype EP2 by PPARγ ligands inhibits human lung carcinoma cell growth |journal=Biochemical and Biophysical Research Communications |date=February 2004 |volume=314 |issue=4 |pages=1093–1099 |doi=10.1016/j.bbrc.2004.01.007|pmid=14751245 }}</ref>

== Prostaglandin E2 and its effect on inflammation ==
Prostaglandins are derived from the parent molecule [[Chemistry:Arachidonic acid|arachidonic acid]]. The synthesis of prostaglandins can be blocked by anti-inflammatory drugs such as [[Chemistry:Ibuprofen|ibuprofen]]. [[Chemistry:Nonsteroidal anti-inflammatory drug|Anti-inflammatory drugs]] block the synthesis of [[Biology:Cyclooxygenase|cyclooxygenases]] which in turn produce prostaglandins.<ref>{{Cite journal  |date=May 2011 |title=Prostaglandins and Inflammation |journal= Arteriosclerosis, Thrombosis, and Vascular Biology|volume=31 |issue=5 |pages=986–1000 |doi=10.1161/ATVBAHA.110.207449 |pmid=21508345 |pmc=3081099 |last1=Ricciotti |first1=Emanuela |last2=Fitzgerald |first2=Garret A. }}</ref> Prostaglandins (PG) are the result of an enzyme cascade pathway that includes two enzymes cyclooxygenase and PG synthase. [[Chemistry:Prostaglandin E2|Prostaglandin E2]] is produced by [[Biology:Prostaglandin E synthase|PGE synthase]] via the activation of EP1-4 receptors. Prostaglandin E2s (PGEs) are associated with the development of vascular diseases that lead to inflammation in the body. In the human body, PGEs are involved in the control of the vascular smooth muscle, cell migration and the division of a cell into two daughter cells.<ref>{{Cite journal |date=22 November 2012 |title=The role of prostaglandin E2 in human vascular inflammation |url=https://www.sciencedirect.com/science/article/abs/pii/S095232781300094X |journal= Prostaglandins, Leukotrienes and Essential Fatty Acids|volume=89 |issue=2–3 |pages=55–63 |doi=10.1016/j.plefa.2013.04.004 |pmid=23756023 |last1=Gomez |first1=I. |last2=Foudi |first2=N. |last3=Longrois |first3=D. |last4=Norel |first4=X. }}</ref> The process of producing two daughter cells via cell division is called [[Biology:Cell proliferation|cell proliferation]]. 

==See also==
* Prostaglandin receptors
* Prostanoid receptors
* Prostaglandin

==References==
{{Reflist|2}}

==External links==
* {{MeshName|Prostaglandin+E2+Receptors}}


{{Transmembrane receptors}}
{{G protein-coupled receptors}}
{{Prostanoidergics}}

[[Category:G protein-coupled receptors]]

{{Sourceattribution|Prostaglandin E2 receptor}}