Editing Prostaglandin

{{short description|Group of physiologically active lipid compounds}}
[[File:Prostaglandin E1.svg|thumb|Chemical structure of [[Prostaglandin E1|prostaglandin E<sub>1</sub>]] (alprostadil)]]
[[File:Prostacyclin-2D-skeletal.png|thumb|175px|Chemical structure of [[Prostacyclin|prostaglandin I<sub>2</sub>]] (prostacyclin)]]

'''Prostaglandins''' ('''PG''') are a group of [[physiology|physiologically]] active [[lipid]] compounds called [[eicosanoid]]s<ref>{{Cite web|url=https://themedicalbiochemistrypage.org/eicosanoids.php|title=Eicosanoid Synthesis and Metabolism: Prostaglandins, Thromboxanes, Leukotrienes, Lipoxins|website=themedicalbiochemistrypage.org|access-date=2018-09-21}}</ref> that have diverse [[hormone]]-like effects in animals.  Prostaglandins have been found in almost every [[Tissue (biology)|tissue]] in humans and other animals. They are derived [[enzymatically]] from the [[fatty acid]] [[arachidonic acid]].<ref name=":0">{{cite journal | vauthors = Ricciotti E, FitzGerald GA | title = Prostaglandins and inflammation | journal = Arteriosclerosis, Thrombosis, and Vascular Biology | volume = 31 | issue = 5 | pages = 986–1000 | date = May 2011 | pmid = 21508345 | pmc = 3081099 | doi = 10.1161/ATVBAHA.110.207449 }}</ref> Every prostaglandin contains 20 [[carbon]] atoms, including a [[carbon ring|5-carbon ring]]. They are a subclass of [[eicosanoid]]s and of the [[prostanoid]] class of fatty acid derivatives.

The structural differences between prostaglandins account for their different biological activities. A given prostaglandin may have different and even opposite effects in different tissues in some cases. The ability of the same prostaglandin to stimulate a reaction in one tissue and inhibit the same reaction in another tissue is determined by the type of [[receptor (biochemistry)|receptor]] to which the prostaglandin binds. They act as [[autocrine]] or [[paracrine]] factors with their target cells present in the immediate vicinity of the site of their [[secretion]]. Prostaglandins differ from [[endocrine system|endocrine]] [[hormone]]s in that they are not produced at a specific site but in many places throughout the human body.

Prostaglandins are powerful, locally-acting [[vasodilator]]s and inhibit the aggregation of blood [[platelets]]. Through their role in vasodilation, prostaglandins are also involved in [[inflammation]]. They are synthesized in the walls of blood vessels and serve the physiological function of preventing needless clot formation, as well as regulating the contraction of [[smooth muscle]] tissue.<ref name="isbn0-87893-617-3">{{cite book | vauthors = Nelson RF |title=An introduction to behavioral endocrinology |edition=3rd |publisher=Sinauer Associates |location=Sunderland, Mass |year=2005 |page=100 |isbn=0-87893-617-3 }}</ref> Conversely, [[thromboxanes]] (produced by platelet cells) are [[vasoconstrictor]]s and facilitate platelet aggregation. Their name comes from their role in clot formation ([[thrombosis]]).

Specific prostaglandins are named with a letter indicating the type of ring structure, followed by a number indicating the number of [[double bond]]s in the [[hydrocarbon]] structure. For example, [[prostaglandin E1|prostaglandin E<sub>1</sub>]] has the abbreviation PGE<sub>1</sub> and [[prostacyclin|prostaglandin I<sub>2</sub>]] has the abbreviation PGI<sub>2</sub>.

== History and name ==
<!-- Deleted image removed: [[File:Ulf-von-Euler.gif|left|frame|Ulf von Euler, a Nobel laureate, discovered and named prostaglandin {{puic|Image:Image_name.ext|log=2008 April 2}}]] -->
Systematic studies of prostaglandins began in 1930, when Kurzrock and Lieb found that human seminal fluid caused either stimulation or relaxation of strips of isolated human uterus. They noted that uteri from patients who had gone through successful pregnancies responded to the fluid with relaxation, while uteri from sterile women responded with contraction.<ref>{{cite journal |last1=Kurzrock |first1=Raphael |last2=Lieb |first2=Charles C. |title=Biochemical Studies of Human Semen. II. The Action of Semen on the Human Uterus |journal=Proceedings of the Society for Experimental Biology and Medicine |date=1930 |volume=28 |issue=3 |page=268 |doi=10.3181/00379727-28-5265 |s2cid=85374636 }}</ref> The name ''prostaglandin'' derives from the [[prostate]] [[gland]], chosen when prostaglandin was first isolated from [[seminal fluid]] in 1935 by the Swedish [[physiology|physiologist]] [[Ulf von Euler]],<ref>{{cite journal | vauthors = Von Euler US |title=Über die spezifische blutdrucksenkende Substanz des menschlichen Prostata- und Samenblasensekrets |trans-title=On the specific blood-pressure-reducing substance of human prostate and seminal vesicle secretions |journal=Wiener Klinische Wochenschrift |volume=14 |issue=33 |pages=1182–1183 |year=1935 |doi=10.1007/BF01778029|s2cid=38622866 }}</ref> and independently by the Irish-English physiologist Maurice Walter Goldblatt (1895–1967).<ref>{{cite journal | vauthors = Goldblatt MW | title = Properties of human seminal plasma | journal = The Journal of Physiology | volume = 84 | issue = 2 | pages = 208–18 | date = May 1935 | pmid = 16994667 | pmc = 1394818 | doi =  10.1113/jphysiol.1935.sp003269| url = http://www.jphysiol.org/cgi/pmidlookup?view=long&pmid=16994667 }}</ref><ref>{{cite book |editor1-last=Rubinstein |editor1-first=William D. |editor2-last=Jolles |editor2-first=Michael A. |editor3-last=Rubinstein |editor3-first=Hillary L. |title=The Palgrave Dictionary of Anglo-Jewish History |date=2011 |publisher=Palgrave Macmillan |location=Basingstoke, England |page=333 |chapter-url=https://books.google.com/books?id=_T_HCg17ufIC&pg=PA333 |chapter=Goldblatt, Maurice Walter|isbn=978-0-230-30466-6 }}</ref><ref>{{cite journal |last1=R.S.F.S. |title=Obituary Notices: M. W. Goldblatt |journal=British Medical Journal |date=3 June 1967 |volume=2 |issue=5552 |page=644 |doi=10.1136/bmj.2.5552.644 |s2cid=220151673 |url=https://www.bmj.com/content/2/5552/644}}</ref> Prostaglandins were believed to be part of the prostatic secretions, and eventually were discovered to be produced by the [[seminal vesicles]]. Later, it was shown that many other tissues secrete prostaglandins and that they perform a variety of functions. The first [[total synthesis|total syntheses]] of [[Prostaglandin F2alpha|prostaglandin F<sub>2α</sub>]] and [[Prostaglandin E2|prostaglandin E<sub>2</sub>]] were reported by [[Elias James Corey]] in 1969,<ref name="Nicolaou">{{cite book |title= Classics in Total Synthesis|url= https://archive.org/details/classicstotalmet00kcni|url-access= limited| vauthors = Nicolaou KC, Sorensen EJ |author-link=K. C. Nicolaou |year= 1996|publisher= VCH|location= Weinheim, Germany|isbn= 3-527-29284-5|page= [https://archive.org/details/classicstotalmet00kcni/page/n90 65] }}</ref> an achievement for which he was awarded the [[Japan Prize]] in 1989.

In 1971, it was determined that [[aspirin]]-like drugs could inhibit the synthesis of prostaglandins. The [[biochemist]]s [[Sune K. Bergström]], [[Bengt I. Samuelsson]] and [[John R. Vane]] jointly received the 1982 [[Nobel Prize in Physiology or Medicine]] for their research on prostaglandins.{{citation needed|date=January 2024}}

== Biochemistry ==

=== Biosynthesis ===
[[File:Eicosanoid synthesis.svg|thumb|300px|[[Biosynthesis]] of eicosanoids]]
Prostaglandins are found in most tissues and organs. They are [[biosynthesis|produced]] by almost all nucleated cells. They are [[autocrine]] and [[paracrine]] lipid mediators that act upon [[platelet]]s, [[endothelium]], [[uterus|uterine]] and [[mast cell]]s. They are synthesized in the cell from the [[fatty acid]] [[arachidonic acid]].<ref name=":0" />

[[Arachidonic acid]] is created from [[diacylglycerol]] via [[phospholipase A2|phospholipase-A<sub>2</sub>]], then brought to either the [[Cyclooxygenase|cyclooxygenase pathway]] or the [[Lipoxygenase|lipoxygenase pathway]]. The cyclooxygenase pathway produces [[thromboxane]], [[prostacyclin]] and prostaglandin D, E and F. Alternatively, the lipoxygenase enzyme pathway is active in [[leukocyte]]s and in [[macrophage]]s and synthesizes [[leukotrienes]].{{citation needed|date=January 2024}}

=== Release of prostaglandins from the cell ===
Prostaglandins were originally believed to leave the cells via passive diffusion because of their high lipophilicity. The discovery of the [[prostaglandin transporter]] (PGT, SLCO2A1), which mediates the cellular uptake of prostaglandin, demonstrated that diffusion alone cannot explain the penetration of prostaglandin through the cellular membrane. The release of prostaglandin has now also been shown to be mediated by a specific transporter, namely the [[multidrug resistance protein 4]] (MRP4, ABCC4), a member of the [[ATP-binding cassette transporter]] superfamily. Whether MRP4 is the only transporter releasing prostaglandins from the cells is still unclear.{{citation needed|date=January 2024}}

==== Cyclooxygenases ====
Prostaglandins are produced following the sequential oxygenation of arachidonic acid, DGLA or EPA by [[cyclooxygenase]]s (COX-1 and COX-2) and terminal prostaglandin syntheses. The classic dogma is as follows:
* [[COX-1]] is responsible for the baseline levels of prostaglandins.
* [[COX-2]] produces prostaglandins through stimulation.

However, while COX-1 and COX-2 are both located in the [[blood vessels]], [[stomach]] and the [[kidneys]], prostaglandin levels are increased by COX-2 in scenarios of [[inflammation]] and [[Human development (biology)|growth]].

==== Prostaglandin E synthase ====
[[Prostaglandin E2|Prostaglandin E<sub>2</sub>]] (PGE<sub>2</sub>) — the most abundant prostaglandin<ref>{{cite journal | vauthors = Ke J, Yang Y, Che Q, Jiang F, Wang H, Chen Z, Zhu M, Tong H, Zhang H, Yan X, Wang X, Wang F, Liu Y, Dai C, Wan X | title = Prostaglandin E2 (PGE2) promotes proliferation and invasion by enhancing SUMO-1 activity via EP4 receptor in endometrial cancer | journal = Tumour Biology | volume = 37 | issue = 9 | pages = 12203–12211 | date = September 2016 | pmid = 27230680 | pmc = 5080328 | doi = 10.1007/s13277-016-5087-x | quote = Prostaglandin E2 (PGE2) is the most abundant prostanoid in the human body }}</ref> — is generated from the action of [[prostaglandin E synthase]]s on prostaglandin H<sub>2</sub> ([[prostaglandin H2]], PGH<sub>2</sub>). Several prostaglandin E syntheses have been identified.  To date, microsomal (named as [[misoprostol]]) prostaglandin E synthase-1 emerges as a key enzyme in the formation of PGE<sub>2</sub>.{{citation needed|date=January 2024}}

==== Other terminal prostaglandin synthases ====
Terminal prostaglandin syntheses have been identified that are responsible for the formation of other prostaglandins. For example, hematopoietic and [[lipocalin]] [[prostaglandin D synthase]]s (hPGDS and lPGDS) are responsible for the formation of [[PGD2|PGD<sub>2</sub>]] from PGH<sub>2</sub>. Similarly, prostacyclin (PGI<sub>2</sub>) synthase (PGIS) converts PGH<sub>2</sub> into PGI<sub>2</sub>. A thromboxane synthase ([[thromboxane-A synthase|TxAS]]) has also been identified.
[[Prostaglandin-F synthase]] (PGFS) catalyzes the formation of 9α,11β-PGF<sub>2α,β</sub> from PGD<sub>2</sub> and PGF<sub>2α</sub> from PGH<sub>2</sub> in the presence of NADPH. This enzyme has recently been crystallized in complex with PGD<sub>2</sub><ref>{{cite journal | vauthors = Komoto J, Yamada T, Watanabe K, Takusagawa F | title = Crystal structure of human prostaglandin F synthase (AKR1C3) | journal = Biochemistry | volume = 43 | issue = 8 | pages = 2188–98 | date = March 2004 | pmid = 14979715 | doi = 10.1021/bi036046x }}</ref> and bimatoprost<ref>{{cite journal | vauthors = Komoto J, Yamada T, Watanabe K, Woodward DF, Takusagawa F | title = Prostaglandin F2alpha formation from prostaglandin H2 by prostaglandin F synthase (PGFS): crystal structure of PGFS containing bimatoprost | journal = Biochemistry | volume = 45 | issue = 7 | pages = 1987–96 | date = February 2006 | pmid = 16475787 | doi = 10.1021/bi051861t }}</ref> (a synthetic analogue of PGF<sub>2α</sub>).

== Functions ==
There are currently ten known [[prostaglandin receptor]]s on various cell types. Prostaglandins ligate a sub-family of cell surface seven-transmembrane receptors, [[G-protein-coupled receptor]]s. These receptors are termed DP1-2, EP1-4, FP, IP1-2, and TP, corresponding to the receptor that ligates the corresponding prostaglandin (e.g., DP1-2 receptors bind to [[PGD2]]).

The diversity of receptors means that prostaglandins act on an array of cells and have a wide variety of effects such as:
* create [[eicosanoid]]s hormones
* act on thermoregulatory center of [[hypothalamus]] to produce [[fever]]
* increase mating behaviors in goldfish<ref>{{Cite web|url=https://www.researchgate.net/publication/226044617|title=Hormonal and pheromonal control of spawning in goldfish (PDF Download Available)|website=ResearchGate|language=en|access-date=2017-02-04}}</ref>
* cause the uterus to contract{{efn|Prostaglandins are released during [[menstruation]], due to the destruction of the [[endometrial]] cells, and the resultant release of their contents.<ref>{{cite journal | vauthors = Lethaby A, Duckitt K, Farquhar C | title = Non-steroidal anti-inflammatory drugs for heavy menstrual bleeding | journal = The Cochrane Database of Systematic Reviews | issue = 1 | pages = CD000400 | date = January 2013 | pmid = 23440779 | doi = 10.1002/14651858.CD000400.pub3 }}</ref>{{Update inline|reason=Updated version https://www.ncbi.nlm.nih.gov/pubmed/31535715|date = November 2019}} Release of prostaglandins and other inflammatory mediators in the [[uterus]] cause the uterus to contract. These substances are thought to be a major factor in primary [[dysmenorrhea]].<ref>Wright, Jason and Solange Wyatt. ''The Washington Manual Obstetrics and Gynecology Survival Guide''. Lippincott Williams & Wilkins, 2003. {{ISBN|0-7817-4363-X}}{{page needed|date=January 2013}}</ref><ref name="Harel 2006">{{cite journal | vauthors = Harel Z | title = Dysmenorrhea in adolescents and young adults: etiology and management | journal = Journal of Pediatric and Adolescent Gynecology | volume = 19 | issue = 6 | pages = 363–71 | date = December 2006 | pmid = 17174824 | doi = 10.1016/j.jpag.2006.09.001 }}</ref><ref>{{cite journal |last1=Bofill Rodriguez |first1=M |last2=Lethaby |first2=A |last3=Farquhar |first3=C |title=Non-steroidal anti-inflammatory drugs for heavy menstrual bleeding. |journal=The Cochrane Database of Systematic Reviews |date=19 September 2019 |volume=2019 |issue=9 |pages=CD000400 |doi=10.1002/14651858.CD000400.pub4 |pmid=31535715|pmc=6751587 }}</ref>}}
* prevent gastrointestinal tract from self-digesting, contributing to its mucosal defence in multifactorial way.<ref>{{Cite journal |last=Wallace |first=John L. |date=October 2008 |title=Prostaglandins, NSAIDs, and Gastric Mucosal Protection: Why Doesn't the Stomach Digest Itself? |url=https://www.physiology.org/doi/10.1152/physrev.00004.2008 |journal=Physiological Reviews |language=en |volume=88 |issue=4 |pages=1547–1565 |doi=10.1152/physrev.00004.2008 |issn=0031-9333}}</ref>

==Types==  <!--PGF2alpha redirects here-->
The following is a comparison of different types of prostaglandin, including [[prostacyclin|prostaglandin I<sub>2</sub>]] (prostacyclin; PGI<sub>2</sub>), [[prostaglandin D2|prostaglandin D<sub>2</sub>]] (PGD<sub>2</sub>), [[prostaglandin E2|prostaglandin E<sub>2</sub>]] (PGE<sub>2</sub>), and [[prostaglandin F2alpha|prostaglandin F<sub>2α</sub>]] (PGF<sub>2α</sub>).<ref>{{cite journal | vauthors = Moreno JJ | title = Eicosanoid receptors: Targets for the treatment of disrupted intestinal epithelial homeostasis | journal = European Journal of Pharmacology | volume = 796 | pages = 7–19 | date = February 2017 | pmid = 27940058 | doi = 10.1016/j.ejphar.2016.12.004 | s2cid = 1513449 }}</ref>

{| class="wikitable"
|-
! Type
! [[Prostaglandin receptor|Receptor]]
! Receptor type
! Function
|-
| '''[[Prostaglandin I2|PGI<sub>2</sub>]]'''
| [[Prostacyclin receptor|IP]]
| [[Gs protein|G<sub>s</sub>]]
|
* [[vasodilation]]
* inhibit [[platelet aggregation]]
* [[bronchodilation]]
|-
| '''[[Prostaglandin D2|PGD<sub>2</sub>]]'''
| [[prostaglandin DP2 receptor|PTGDR (DP1) and CRTH2 (DP2)]]
| [[GPCR]]
|
* produced by mast cells; recruits Th2 cells, eosinophils, and basophils
* In [[mammal]]ian organs, large amounts of PGD2 are found only in the brain and in mast cells
* Critical to development of allergic diseases such as asthma
|-
| rowspan=4 | '''[[Prostaglandin E2|PGE<sub>2</sub>]]'''
| [[Prostaglandin EP1 receptor|EP<sub>1</sub>]]
| [[Gq protein|G<sub>q</sub>]]
|
* [[bronchoconstriction]]
* [[GI tract]] [[smooth muscle]] contraction
* enhanced proliferation of [[T lymphocytes]] (Th1 sub-type)
|-
| [[Prostaglandin E2 receptor|EP<sub>2</sub>]]
| [[Gs protein|G<sub>s</sub>]]
|
* [[bronchodilation]]
* [[GI tract]] [[smooth muscle]] relaxation
* [[vasodilation]]
* reduced intra-ocular pressure
* regulation of [[B cells]], [[T cells]] (CD4 & CD8) & [[antigen presenting cell]] function
* pro-inflammatory cell development → inflammation & fever
* suppression of [[NMDA receptor]] related neurotoxicity (only present within the central nervous system)
|-
| [[Prostaglandin EP3 receptor|EP<sub>3</sub>]]
| [[Gi protein|G<sub>i</sub>]]
|
* [[uterus]] contraction (when pregnant)
* [[GI tract]] [[smooth muscle]] contraction
* [[lipolysis]] inhibition
* inhibitory effect on thermogenic pre-optic hypothalamus
* stimulate nitrix oxide synthesis → PGE2 synthesis → pyogenic
* ↑ mast cell release of histamine (increasing allergy response)
* ↑ pain perception
* hyperalgesia (wild type EP3 expression)
* ↑ [[autonomous ns|autonomic]] [[neurotransmitters]]<ref name=Rang>{{cite book | vauthors = Rang HP |title=Pharmacology |publisher=Churchill Livingstone |location=Edinburgh |year=2003 |page=234 |isbn=0-443-07145-4 |edition=5th }}</ref>
* ↑ platelet response to their agonists<ref>{{cite journal | vauthors = Fabre JE, Nguyen M, Athirakul K, Coggins K, McNeish JD, Austin S, Parise LK, FitzGerald GA, Coffman TM, Koller BH | title = Activation of the murine EP3 receptor for PGE2 inhibits cAMP production and promotes platelet aggregation | journal = The Journal of Clinical Investigation | volume = 107 | issue = 5 | pages = 603–10 | date = March 2001 | pmid = 11238561 | pmc = 199422 | doi = 10.1172/JCI10881 }}</ref> and ↑ atherothrombosis in vivo<ref>{{cite journal | vauthors = Gross S, Tilly P, Hentsch D, Vonesch JL, Fabre JE | title = Vascular wall-produced prostaglandin E2 exacerbates arterial thrombosis and atherothrombosis through platelet EP3 receptors | journal = The Journal of Experimental Medicine | volume = 204 | issue = 2 | pages = 311–20 | date = February 2007 | pmid = 17242161 | pmc = 2118736 | doi = 10.1084/jem.20061617 }}</ref>
|-
| [[Prostaglandin EP4 receptor|EP<sub>4</sub>]]
| [[Gs protein|G<sub>s</sub>]]
|
* [[hyperalgesia]]<ref name=Rang/>
* [[Fever|pyrogenic]]
* supports regulatory T cell production
* stimulate [[dendritic cell]] maturation ([[antigen presenting cells]] of skin & mucosa)
* inhibit antibody B cell proliferation
* ↑ inflammatory region blood flow (pyogenic & [[erythema]])
* Inhibitory effects of [[dorsal root ganglion]] (speculated reduction in [[allodynia]] & hyperalgesia)
* ↓ [[stomach|gastric]] acid secretion
* ↑ [[stomach|gastric]] [[mucus]] secretion
* Prostate cancer (↑ EP4 expression)
* ↑ corneal [[neovascularization]]
* ↑ chohlea auditory brain stem response
|-
| '''[[Prostaglandin F2alpha|PGF<sub>2α</sub>]]'''
| [[Prostaglandin F receptor|FP]]
| [[Gq protein|G<sub>q</sub>]]
|
* [[uterus]] contraction
* [[bronchoconstriction]]
* urinary bladder contractions<ref>{{cite journal |last1=Stromberga |first1=Zane |last2=Chess-Williams |first2=Russ |last3=Moro |first3=Christian |title=Prostaglandin E2 and F2alpha Modulate Urinary Bladder Urothelium, Lamina Propria and Detrusor Contractility via the FP Receptor |journal=Frontiers in Physiology |date=23 June 2020 |volume=11 |page=705 |doi=10.3389/fphys.2020.00705 |pmid=32714206 |pmc=7344237 |doi-access=free }}</ref>
* vasoconstriction in cerebral circulation<ref>{{cite book |doi=10.1016/B978-0-323-05908-4.10007-7 |chapter=Cerebral and Spinal Cord Blood Flow |title=Cottrell and Young's Neuroanesthesia |year=2010 |last1=Joshi |first1=Shailendra |last2=Ornstein |first2=Eugene |last3=Young |first3=William L. |pages=17–59 |isbn=978-0-323-05908-4 }}</ref>
|}

== Role in pharmacology ==

===Inhibition===
{{see also|Prostaglandin antagonist|Mechanism of action of aspirin}}

Examples of prostaglandin antagonists are:
* [[NSAID]]s (inhibit [[cyclooxygenase]]) and [[COX-2 selective inhibitors]] or coxibs
* [[Corticosteroids]] (inhibit [[phospholipase A2|phospholipase A<sub>2</sub>]] production)
* [[Cyclopentenone prostaglandin]]s may play a role in inhibiting [[inflammation]]
* [[Vitamin D3|Vitamin D<sub>3</sub>]] and [[Vitamin K2|vitamin K<sub>2</sub>]].<ref name="pmid34206530">{{cite journal| author=Kieronska-Rudek A, Kij A, Kaczara P, Tworzydlo A, Napiorkowski M, Sidoryk K | display-authors=etal| title=Exogenous Vitamins K Exert Anti-Inflammatory Effects Dissociated from Their Role as Substrates for Synthesis of Endogenous MK-4 in Murine Macrophages Cell Line. | journal=Cells | year= 2021 | volume= 10 | issue= 7 | page=1571| pmid=34206530 | doi=10.3390/cells10071571 | pmc=8303864 | doi-access=free}}</ref><ref name="pmid8240383">{{cite journal| author=Koshihara Y, Hoshi K, Shiraki M| title=Vitamin K2 (menatetrenone) inhibits prostaglandin synthesis in cultured human osteoblast-like periosteal cells by inhibiting prostaglandin H synthase activity. | journal=Biochem Pharmacol | year= 1993 | volume= 46 | issue= 8 | pages= 1355–62 | pmid=8240383 | doi=10.1016/0006-2952(93)90099-i }}</ref><ref name="pmid20046582">{{cite journal| author=Krishnan AV, Srinivas S, Feldman D| title=Inhibition of prostaglandin synthesis and actions contributes to the beneficial effects of calcitriol in prostate cancer. | journal=Dermatoendocrinol | year= 2009 | volume= 1 | issue= 1 | pages= 7–11 | pmid=20046582 | doi=10.4161/derm.1.1.7106 | pmc=2715203 }}</ref>

===Clinical uses===
Synthetic prostaglandins are used:
* To induce [[childbirth]] (parturition) or [[abortion]] (PGE<sub>2</sub> or PGF<sub>2(misoprostol)</sub>, with or without [[mifepristone]], a progesterone antagonist)
** [[Induction of labour]]<ref name="NCBI Bookshelf WHO">{{cite web | title=WHO Recommendations for Induction of Labour | website=NCBI Bookshelf | url=https://www.ncbi.nlm.nih.gov/books/NBK131965/ | access-date=2020-07-15 | quote= Induction of labour is defined as the process of artificially stimulating the uterus to start labour (1). It is usually performed by administering oxytocin or prostaglandins to the pregnant woman or by manually rupturing the amniotic membranes.}}</ref>
* To prevent closure of [[ductus arteriosus]] in newborns with particular [[cyanotic heart defect]]s (PGE<sub>1</sub>)
* As a [[vasodilation|vasodilator]] in severe [[Raynaud syndrome]] or [[ischemia]] of a limb
* In [[pulmonary hypertension]]
* In treatment of [[glaucoma]] (as in [[bimatoprost]] ophthalmic solution, a synthetic prostamide analog with ocular hypotensive activity) (PGF<sub>2α</sub>)
* To treat [[erectile dysfunction]] or in penile rehabilitation following surgery (PGE1 as [[alprostadil]]).<ref name="muse">Medscape ''[http://www.medscape.com/viewarticle/515218 Early Penile Rehabilitation Helps Reduce Later Intractable ED]''</ref>
* To measure erect [[penis size]] in a clinical environment<ref name=veale2015>{{cite journal |doi=10.1111/bju.13010 |doi-access=free |pmid=25487360 |title=Am I normal? A systematic review and construction of nomograms for flaccid and erect penis length and circumference in up to 15 521 men |journal=BJU International |volume=115 |issue=6 |pages=978–986 |year=2015 |last1=Veale |first1=David |last2=Miles |first2=Sarah |last3=Bramley |first3=Sally |last4=Muir |first4=Gordon |last5=Hodsoll |first5=John}}</ref>
* To treat [[egg binding]] in small [[bird]]s<ref>{{cite web |url=http://www.michvma.org/documents/MVC%20Proceedings/Labonde2.pdf |title=Avian Reproductive and Pediatric Disorders |access-date=2008-01-26 |last=LaBonde, MS, DVM |first=Jerry| publisher=Michigan Veterinary Medical Association |archive-url = https://web.archive.org/web/20080227041626/http://www.michvma.org/documents/MVC%20Proceedings/Labonde2.pdf <!-- Bot retrieved archive --> |archive-date = 2008-02-27}}</ref>

==Synthesis==
The original synthesis of prostaglandins F2α and E2 is shown below.  It involves a Diels–Alder reaction which establishes the relative stereochemistry of three contiguous stereocenters on the prostaglandin cyclopentane core.<ref>{{cite journal |last1=Corey |first1=E. J. |last2=Weinshenker |first2=N. M. |last3=Schaaf |first3=T. K. |last4=Huber |first4=W. |year=1969 |title=Stereo-controlled synthesis of prostaglandins F-2a and E-2 (dl)|journal=Journal of the American Chemical Society |volume=91 |issue=20 |pages=5675–7 |doi=10.1021/ja01048a062 |pmid=5808505}}</ref>

[[File:Prostaglandin Diels-Alder Corey.png|800x325 px|Diels-Alder in the total synthesis of prostaglandin F2α by E. J. Corey|center]]

== Prostaglandin stimulants ==
Cold exposure and IUDs may increase prostaglandin production.<ref name="Handbook of Applied Therapeutics">{{cite book |author=Mary Anne Koda-Kimble |title=Handbook of Applied Therapeutics | edition=8th |language=en |publisher=Lippincott Williams & Wilkins |year=2007 |page=1104 |isbn=978-0-7817-9026-0 }}</ref>

== See also ==
* [[Oxaprostaglandin]], a type of prostaglandin
* [[Prostamide]]s, a chemically related class of physiologically active substances

== Notes ==
{{notelist}}

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

== External links ==
* {{MeshName|Prostaglandins}}

{{Hormones}}
{{Eicosanoids}}
{{Oxytocics}}
{{Drugs for peptic ulcer and GORD}}
{{Antiglaucoma preparations and miotics}}
{{Urologicals}}
{{Prostanoidergics}}
{{Authority control}}

[[Category:Prostaglandins| ]]