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{{short description|Group of physiologically active lipid compounds}}
A '''prostaglandin''' is any member of a group of ] compounds that are derived from ]s and have important functions in the ] body. Every prostaglandin contains 20 ] atoms, including a 5-carbon ring.
] (alprostadil)]]
They are mediators and have a variety of strong ] effects; although they are technically ]s, they are rarely classified as such.
] (prostacyclin)]]


'''Prostaglandins''' ('''PG''') are a group of ] active ] compounds called ]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 ]-like effects in animals. Prostaglandins have been found in almost every ] in humans and other animals. They are derived ] from the ] ].<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 ] atoms, including a ]. They are a subclass of ]s and of the ] class of fatty acid derivatives.
The prostaglandins together with the ]s form the ] class of fatty acid derivatives; the prostanoid class is a subclass of ]s.

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 ] to which the prostaglandin binds. They act as ] or ] factors with their target cells present in the immediate vicinity of the site of their ]. Prostaglandins differ from ] ]s in that they are not produced at a specific site but in many places throughout the human body.

Prostaglandins are powerful, locally-acting ]s and inhibit the aggregation of blood ]. Through their role in vasodilation, prostaglandins are also involved in ]. 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 ] 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, ] (produced by platelet cells) are ]s and facilitate platelet aggregation. Their name comes from their role in clot formation (]).

Specific prostaglandins are named with a letter indicating the type of ring structure, followed by a number indicating the number of ]s in the ] structure. For example, ] has the abbreviation PGE<sub>1</sub> and ] has the abbreviation PGI<sub>2</sub>.


== History and name == == History and name ==
<!-- Deleted image removed: ] -->
The name ''prostaglandin'' derives from the ]. When prostaglandin was first isolated from ] in ], it was believed to be part of the prostatic secretions. In ], it was determined that ]-like drugs could inhibit the synthesis of prostaglandins. The biochemists ], ] and ] jointly received the ] ] for their research on prostaglandins.
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 ] ], chosen when prostaglandin was first isolated from ] in 1935 by the Swedish ] ],<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 ]. Later, it was shown that many other tissues secrete prostaglandins and that they perform a variety of functions. The first ] of ] and ] were reported by ] 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= }}</ref> an achievement for which he was awarded the ] in 1989.

In 1971, it was determined that ]-like drugs could inhibit the synthesis of prostaglandins. The ]s ], ] and ] jointly received the 1982 ] for their research on prostaglandins.{{cn|date=January 2024}}


== Biochemistry == == Biochemistry ==

=== Biosynthesis === === Biosynthesis ===
] of eicosanoids]]
]Prostaglandins are found in virtually all tissues and organs. These are ] and ] lipid mediators that act upon ], ], ] and ]s, among others. They are synthesized in the cell from the essential fatty acids {{ref|merck}}
Prostaglandins are found in most tissues and organs. They are ] by almost all nucleated cells. They are ] and ] lipid mediators that act upon ]s, ], ] and ]s. They are synthesized in the cell from the ] ].<ref name=":0" />
* ] (GLA, an omega-6 EFA) - yielding the series-1 prostaglandins

* ] (AA, omega-6) - yielding series-2
] is created from ] via ], then brought to either the ] or the ]. The cyclooxygenase pathway produces ], ] and prostaglandin D, E and F. Alternatively, the lipoxygenase enzyme pathway is active in ]s and in ]s and synthesizes ].{{cn|date=January 2024}}
* ] (EPA, omega-3) - yielding series-3

An intermediate is created by ], then passed into one of either the ] or the ] to form either prostaglandin and thromboxane or ]. The cyclooxygenase pathway produces ], ] and prostaglandin D, E and F. The lipoxygenase pathway is active in ]s and in ]s and synthesises leukotrienes. Prostaglandins are released through the prostaglandin transporter on the cell's plasma membrane.
=== 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 ] (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 ] (MRP4, ABCC4), a member of the ] superfamily. Whether MRP4 is the only transporter releasing prostaglandins from the cells is still unclear.{{cn|date=January 2024}}


==== Cyclooxygenases ==== ==== Cyclooxygenases ====
Prostaglandins are produced following the sequential of AA, GLA or EPA by ]s (COX-1 and COX-2) and terminal prostaglandin synthases. The classic dogma is that COX-1 is responsible for the baseline levels of prostaglandins, whereas COX-2 produces prostaglandins through stimulation. However, while COX-1 and COX-2 are both located in the ], ] and the ], prostaglandin level are induced by COX-2 in scenarios of ]. Prostaglandins are produced following the sequential oxygenation of arachidonic acid, DGLA or EPA by ]s (COX-1 and COX-2) and terminal prostaglandin synthases. The classic dogma is as follows:
* ] is responsible for the baseline levels of prostaglandins.
* ] produces prostaglandins through stimulation.
However, while COX-1 and COX-2 are both located in the ], ] and the ], prostaglandin levels are increased by COX-2 in scenarios of ] and ].


==== Prostaglandin E synthase ==== ==== Prostaglandin E synthase ====
Prostaglandin (PG) E2 is generated from the action of prostaglandin E synthases on prostaglandin H2 (PGH2). Several prostaglandin E synthases have been identified. To date, microsomal prostaglandin E synthase-1 emerges as a key enzyme in the formation of PGE2. ] (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 ]s on prostaglandin H<sub>2</sub> (], PGH<sub>2</sub>). Several prostaglandin E synthases have been identified. To date, microsomal (named as ]) prostaglandin E synthase-1 emerges as a key enzyme in the formation of PGE<sub>2</sub>.{{cn|date=January 2024}}


==== Other terminal prostaglandin synthases ==== ==== Other terminal prostaglandin synthases ====
Terminal prostaglandin synthases have been identified that are responsible for the formation of other prostaglandins. For example, hematopoietic and lipocailin prostaglandin D synthases (hPGDS and lPGDS) are responsible for the formation of PGD2 from PGH2. Similarly, prostacyclin (PGI2) synthase (PGIS) converts PGH2 into PGI2. A thromboxane synthase (TxAS) has also been idenfitied. While there is evidence that a prostaglandin F synthase (PGFS) may exist, the evidence remains controversial. Terminal prostaglandin synthases have been identified that are responsible for the formation of other prostaglandins. For example, hematopoietic and ] ]s (hPGDS and lPGDS) are responsible for the formation of ] 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 (]) has also been identified.
] (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>).


=== Function === == Functions ==
There are currently nine known receptors of prostaglandins on various cell types. Prostaglandins ligate a subfamily of cell surface seven transmembrane receptors ]s. These receptors are termed DP1-2, EP1-4, FP, IP, and TP, corresponding to the receptor that ligates the corresponding prostaglandin (e.g., DP1-2 receptors bind to PGD2). Prostaglandins thus act on a variety of cells such as ] cells causing constriction or dilation, on ]s causing aggregation or disaggregation and on spinal ]s causing pain. Prostaglandins have a wide variety of actions, including, but not limited to ] constriction and mediate inflammation. Other effects include ] movement, ] regulation and ] control. Thromboxane is created in ]s and causes ] and platelet aggregation. ] comes from cells in the blood vessel walls and is antagonistic to thromboxane. There are currently ten known ]s on various cell types. Prostaglandins ligate a sub-family of cell surface seven-transmembrane receptors, ]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 ]).


The diversity of receptors means that prostaglandins act on an array of cells and have a wide variety of effects such as:
Prostaglandins are potent but have a short half-life before being inactivated and excreted. Therefore, they exert only a ] (locally active) or ] (acting on the same cell from which it is synthesized) function.
* create ]s hormones
* act on thermoregulatory center of ] to produce ]
* 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 ], due to the destruction of the ] 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 ] cause the uterus to contract. These substances are thought to be a major factor in primary ].<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-->
15-deoxy-&#916;<sup>12,14</sup>-PGJ<sub>2</sub> (15d-PGJ<sub>2</sub>) is a PGD<sub>2</sub> derivative that acts on ] intracellular receptors.
The following is a comparison of different types of prostaglandin, including ] (prostacyclin; PGI<sub>2</sub>), ] (PGD<sub>2</sub>), ] (PGE<sub>2</sub>), and ] (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
! ]
! Receptor type
! Function
|-
| ''']'''
| ]
| ]
|
* ]
* inhibit ]
* ]
|-
| ''']'''
| ]
| ]
|
* produced by mast cells; recruits Th2 cells, eosinophils, and basophils
* In ]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 | ''']'''
| ]
| ]
|
* ]
* ] ] contraction
* enhanced proliferation of ] (Th1 sub-type)
|-
| ]
| ]
|
* ]
* ] ] relaxation
* ]
* reduced intra-ocular pressure
* regulation of ], ] (CD4 & CD8) & ] function
* pro-inflammatory cell development → inflammation & fever
* supression of ] related neurotoxicity (only present within the central nervous system)
|-
| ]
| ]
|
* ] contraction (when pregnant)
* ] ] contraction
* ] 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)
* ↑ ] ]<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>
|-
| ]
| ]
|
* ]<ref name=Rang/>
* ]
* supports regulatory T cell production
* stimulate ] maturation (] of skin & mucosa)
* inhibit antibody B cell proliferation
* ↑ inflammatory region blood flow (pyogenic & ])
* Inhibitory effects of ] (speculated reduction in ] & hyperalgesia)
* ↓ ] acid secretion
* ↑ ] ] secretion
* Prostate cancer (↑ EP4 expression)
* ↑ corneal ]
* ↑ chohlea auditory brain stem response
|-
| ''']'''
| ]
| ]
|
* ] contraction
* ]
* 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 == == Role in pharmacology ==
]s inhibit cyclooxygenase and reduce prostaglandin synthesis. ]s inhibit phospholipase A<sub>2</sub> production by boosting production of ], an inhibitor protein. Relatively new drugs, known as ]s or coxibs, are used as specific inhibitors of COX-2 (Coxibs). The development of these drugs allowed the circumvention of the negative gastrointestinal effects while effectively reducing inflammation. However, recently, it has been shown that both NSAIDs and Coxibs can raise the risk of ], when taken on a chronic basis for at least 18 months. One emerging hypothesis that may explain the cardiovascular effects is that coxibs create an imbalance in circulating TxA2 and PGI2 levels. An increased in the ratio of TxA2/PGI2 could lead to increased platelet aggregation and dysregulation of platelet homeostatis.


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

Examples of prostaglandin antagonists are:
* ]s (inhibit ]) and ] or coxibs
* ] (inhibit ] production)
* ]s may play a role in inhibiting ]
* ] and ].<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: Synthetic prostaglandins are used:
* to induce ] or ] (PGE<sub>2</sub> or PGF<sub>2</sub>, with ]); * To induce ] (parturition) or ] (PGE<sub>2</sub> or PGF<sub>2(misoprostol)</sub>, with or without ], a progesterone antagonist)
** ]<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 ] in newborns with particular ]s
* to prevent and treat ]s (PGE) * To prevent closure of ] in newborns with particular ]s (PGE<sub>1</sub>)
* as a ] in severe ] or ] of a limb * As a ] in severe ] or ] of a limb
* in ] * In ]
* in treatment of ] (as in bimatoprost ophthalmic solution, a synthetic prostamide analog with ocular hypotensive activity) * In treatment of ] (as in ] 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|muse}} * To treat ] or in penile rehabilitation following surgery (PGE1 as ]).<ref name="muse">Medscape ''''</ref>
* To measure erect ] 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 ] in small ]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>

]

== 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 ==
* ], a type of prostaglandin
* ]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}}
]


]
==External links==
# {{note|merck}} Dorlands Medical Dictionary URL reference on 10/23/05.
# {{note|muse}} Medscape <i>Early Penile Rehabilitation Helps Reduce Later Intractable ED</i> URL reference on 10/23/05.

Latest revision as of 01:15, 14 January 2025

Group of physiologically active lipid compounds
Chemical structure of prostaglandin E1 (alprostadil)
Chemical structure of prostaglandin I2 (prostacyclin)

Prostaglandins (PG) are a group of physiologically active lipid compounds called eicosanoids that have diverse hormone-like effects in animals. Prostaglandins have been found in almost every tissue in humans and other animals. They are derived enzymatically from the fatty acid arachidonic acid. Every prostaglandin contains 20 carbon atoms, including a 5-carbon ring. They are a subclass of eicosanoids 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 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 hormones in that they are not produced at a specific site but in many places throughout the human body.

Prostaglandins are powerful, locally-acting vasodilators 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. Conversely, thromboxanes (produced by platelet cells) are vasoconstrictors 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 bonds in the hydrocarbon structure. For example, prostaglandin E1 has the abbreviation PGE1 and prostaglandin I2 has the abbreviation PGI2.

History and name

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. The name prostaglandin derives from the prostate gland, chosen when prostaglandin was first isolated from seminal fluid in 1935 by the Swedish physiologist Ulf von Euler, and independently by the Irish-English physiologist Maurice Walter Goldblatt (1895–1967). 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 syntheses of prostaglandin F2α and prostaglandin E2 were reported by Elias James Corey in 1969, 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 biochemists 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.

Biochemistry

Biosynthesis

Biosynthesis of eicosanoids

Prostaglandins are found in most tissues and organs. They are produced by almost all nucleated cells. They are autocrine and paracrine lipid mediators that act upon platelets, endothelium, uterine and mast cells. They are synthesized in the cell from the fatty acid arachidonic acid.

Arachidonic acid is created from diacylglycerol via phospholipase-A2, then brought to either the cyclooxygenase pathway or the lipoxygenase pathway. The cyclooxygenase pathway produces thromboxane, prostacyclin and prostaglandin D, E and F. Alternatively, the lipoxygenase enzyme pathway is active in leukocytes and in macrophages and synthesizes leukotrienes.

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.

Cyclooxygenases

Prostaglandins are produced following the sequential oxygenation of arachidonic acid, DGLA or EPA by cyclooxygenases (COX-1 and COX-2) and terminal prostaglandin synthases. 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 growth.

Prostaglandin E synthase

Prostaglandin E2 (PGE2) — the most abundant prostaglandin — is generated from the action of prostaglandin E synthases on prostaglandin H2 (prostaglandin H2, PGH2). Several prostaglandin E synthases have been identified. To date, microsomal (named as misoprostol) prostaglandin E synthase-1 emerges as a key enzyme in the formation of PGE2.

Other terminal prostaglandin synthases

Terminal prostaglandin synthases have been identified that are responsible for the formation of other prostaglandins. For example, hematopoietic and lipocalin prostaglandin D synthases (hPGDS and lPGDS) are responsible for the formation of PGD2 from PGH2. Similarly, prostacyclin (PGI2) synthase (PGIS) converts PGH2 into PGI2. A thromboxane synthase (TxAS) has also been identified. Prostaglandin-F synthase (PGFS) catalyzes the formation of 9α,11β-PGF2α,β from PGD2 and PGF2α from PGH2 in the presence of NADPH. This enzyme has recently been crystallized in complex with PGD2 and bimatoprost (a synthetic analogue of PGF2α).

Functions

There are currently ten known prostaglandin receptors on various cell types. Prostaglandins ligate a sub-family of cell surface seven-transmembrane receptors, G-protein-coupled receptors. 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 eicosanoids hormones
  • act on thermoregulatory center of hypothalamus to produce fever
  • increase mating behaviors in goldfish
  • cause the uterus to contract
  • prevent gastrointestinal tract from self-digesting, contributing to its mucosal defence in multifactorial way.

Types

The following is a comparison of different types of prostaglandin, including prostaglandin I2 (prostacyclin; PGI2), prostaglandin D2 (PGD2), prostaglandin E2 (PGE2), and prostaglandin F2α (PGF2α).

Type Receptor Receptor type Function
PGI2 IP Gs
PGD2 PTGDR (DP1) and CRTH2 (DP2) GPCR
  • produced by mast cells; recruits Th2 cells, eosinophils, and basophils
  • In mammalian organs, large amounts of PGD2 are found only in the brain and in mast cells
  • Critical to development of allergic diseases such as asthma
PGE2 EP1 Gq
EP2 Gs
EP3 Gi
  • 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)
  • ↑ autonomic neurotransmitters
  • ↑ platelet response to their agonists and ↑ atherothrombosis in vivo
EP4 Gs
PGF2α FP Gq

Role in pharmacology

Inhibition

See also: Prostaglandin antagonist and Mechanism of action of aspirin

Examples of prostaglandin antagonists are:

Clinical uses

Synthetic prostaglandins are used:

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.

Diels-Alder in the total synthesis of prostaglandin F2α by E. J. Corey
Diels-Alder in the total synthesis of prostaglandin F2α by E. J. Corey

Prostaglandin stimulants

Cold exposure and IUDs may increase prostaglandin production.

See also

Notes

  1. Prostaglandins are released during menstruation, due to the destruction of the endometrial cells, and the resultant release of their contents. 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.

References

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DP (D2)Tooltip Prostaglandin D2 receptor
DP1Tooltip Prostaglandin D2 receptor 1
DP2Tooltip Prostaglandin D2 receptor 2
EP (E2)Tooltip Prostaglandin E2 receptor
EP1Tooltip Prostaglandin EP1 receptor
EP2Tooltip Prostaglandin EP2 receptor
EP3Tooltip Prostaglandin EP3 receptor
EP4Tooltip Prostaglandin EP4 receptor
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PGD2STooltip Prostaglandin D synthase
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Receptor/signaling modulators
Leukotriene signaling modulators
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