prostacyclin

(redirected from PGI2)
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Related to PGI2: prostaglandin, PGF2, PGD2

pros·ta·cy·clin

 (prŏs′tə-sī′klĭn)
n.
A prostaglandin produced in the walls of blood vessels that acts as a vasodilator and inhibits platelet aggregation.

American Heritage® Dictionary of the English Language, Fifth Edition. Copyright © 2016 by Houghton Mifflin Harcourt Publishing Company. Published by Houghton Mifflin Harcourt Publishing Company. All rights reserved.

prostacyclin

(ˌprɒstəˈsaɪklɪn)
n
(Biochemistry) biochem any of several prostaglandins produced in the blood vessels, causing vasodilation and inhibiting platelet aggregation
Collins English Dictionary – Complete and Unabridged, 12th Edition 2014 © HarperCollins Publishers 1991, 1994, 1998, 2000, 2003, 2006, 2007, 2009, 2011, 2014

pros•ta•cy•clin

(ˌprɒs təˈsaɪ klɪn)

n.
a prostaglandin, C20H32O5, that specifically inhibits the formation of blood clots.
[1975–80; prosta (te) + cycl (ic) + -in1, on the model of prostaglandin]
Random House Kernerman Webster's College Dictionary, © 2010 K Dictionaries Ltd. Copyright 2005, 1997, 1991 by Random House, Inc. All rights reserved.
References in periodicals archive ?
The presence of an inverse relationship between circulating [Mg.sup.2+] levels and the detected concentrations of endothelin-1, PGI2, ROS, NO, or renin, or systolic and diastolic blood pressure values, however, leaves unanswered the question as to whether magnesium supplementation can be therapeutic in restoring physiological and age-appropriate pressure values.
Abbreviations C-section: Cesarean section TIPS: Transjugular intrahepatic portosystemic shunt ATII: Angiotensin II PGI2: Prostaglandin I2 IVC: Inferior vena cava STI: Sexually transmitted infection HPV: Human papilloma virus NASH: Nonalcoholic fatty liver disease.
And the stimulating process of ET-1 synthesis needs the involvement of Ca2+ (dependent protein kinase C).19 Factors that inhibit ET-1 synthesis include NO, PGI2, atrial natriuretic peptide, heparin, etc.
The following four aspects might be important for the effects of vitamin D on atherosclerosis: (1) Vitamin D can increase the expression of Ca-ATRase in vascular endothelial cells and smooth muscle cells, elevate cytosolic free calcium concentrations, induce contractile proteins expression, and then promote production of prostacyclin (PGI2), which affects the vascular tone; Vitamin D can improve endothelial function by inhibiting the inflammatory reaction and oxidative injury [17,18], and it can decrease vascular stiffness [19].
In contrast, the imbalance in PGI2 and TX[A.sub.2] production is involved in the pathophysiology of myocardial infarction, atherosclerosis, and CI [23, 26, 27].
AEC: alveolar epithelial cell; CCL: C-C motif chemokine ligand; CD40L: CD40 ligand; CXCL: C-X-C motif chemokine ligand; ECAM: endothelial cell adhesion molecule; FGF: fibroblast growth factor; HDAC: histone deacetylase; GM-CSF: granulocyte macrophage colony stimulating factor; HIF: hypoxia-inducible factor; ICAM: intercellular adhesion molecule; IL: interleukin; NO-sGC-cGMP: nitric oxide-soluble guanylate cyclase-cyclic GMP; MCP: monocyte chemoattractant protein; PDGF: platelet-derived growth factor; PGI2: prostacyclin; RANTES: regulated upon activation, normally T-expressed, and presumably secreted; ROS: reactive oxygen species; SDF: stromal cell-derived factor; TRPC6: transient receptor potential cation channel 6; VCAM: vascular cell adhesion molecule.
O'Grady, "Side effects occurring during administration of epoprostenol (prostacyclin, PGI2), in man.," British Journal of Clinical Pharmacology, vol.
This enzyme, now called COX-1, is central to AA catabolism to end up producing PGI2, also known as prostacyclin, with clear antithrombogenic [8, 9] and cytoprotective to gastric mucosa [10,11] physiological functions.
The whole blood was supplemented with prostacyclin (PGI2) at the final concentration of 0.06 f g/ml, and centrifuged for 20 minutes at 230 xg at 21[degrees]C in order to obtain PRP.
Expression of LIF mRNA was used in three studies, expression of LIF protein, and implantation sites were used in two studies, and COX-2, IFN-[gamma], IL-10, integrin [alpha][nu] mRNA, integrin [beta]3 proteins, LIF mRNA/[beta]-actin, MMP-9, NF-[kappa]BOPN mRNA, PGI2, PPARd, IL-11 mRNA, TIMP-3, apoptotic index, proliferative index, LCM-DE-MS, microvessel density, endometrial thickness, and pinopodes in the epithelium were used in one study (Table 1).
These mediators can be divided into two types: (1) vasodilators, such as endothelium-derived relaxing factors (EDRFs), nitric oxide (NO), prostacyclin (PGI2) [8], and endothelium-derived hyperpolarizing factors (EDHFs) [13-16], and (2) vasoconstrictors, which include endothelin-1, reactive oxygen species (ROS), platelet-activating factor (PAF) [8], and arachidonic acid (AA) cyclooxygenase-derived metabolites [17].